Venous Congestion, Organ Perfusion, and Tissue Edema

Blood must leave an organ as well as enter it. When pressure rises in the draining veins, blood has less pressure available to move through the organ. The same venous pressure rise can also increase tissue swelling. These mechanisms help explain why organ function can deteriorate despite an apparently adequate arterial pressure.

19.1 Congestion Is Related to Pressure, Volume, and Vascular Capacity

Venous congestion develops when blood accumulates on the venous side of the circulation and the resulting pressure impairs drainage or organ function. To understand it, distinguish the amount of fluid in the body from the pressure within its vessels. Positive fluid balance describes retained fluid. It does not directly measure venous pressure or show which organs are affected.

The veins can hold a large volume because their walls expand relatively easily. Venous compliance describes how much their volume changes for a given change in distending pressure. A highly compliant vein can accept additional blood with a small pressure increase. When the vessel becomes less compliant, the same added volume produces a larger pressure rise.

Venous capacity also changes when smooth muscle contracts. Venoconstriction reduces the volume that reservoir veins can hold at a given pressure. Blood shifts toward the central circulation even though no fluid has entered the body. Venodilation has the opposite effect: more blood remains in the peripheral reservoir, and less contributes to the pressure driving venous return. This can occur in a patient who already has excess extracellular fluid.

The heart must then accept and eject the returning blood. If the right ventricle cannot move that blood through the pulmonary circulation, right atrial pressure rises. Pressure is transmitted upstream into the systemic veins. Increased pulmonary vascular resistance, severe right ventricular dysfunction, and restriction by the pericardium can therefore produce congestion through impaired cardiac filling or emptying. Fluid retention may worsen the problem, but it need not be the initiating event.

Obstruction can also occur farther from the heart. Renal vein thrombosis can impair one kidney's drainage. Portal venous obstruction can affect the splanchnic circulation. An obstructed limb vein can cause unilateral swelling. These regional problems may be severe even when central venous pressure is not elevated.

Keep three observations distinct. Fluid accumulation describes the body's retained water and solute. Venous hypertension describes increased pressure. Organ congestion describes the regional consequences of venous filling, pressure transmission, and impaired drainage. A patient can have all three, but their severity need not change together.

This distinction changes the interpretation of a swollen patient with poor forward flow. The edema does not show how rapidly tissue fluid can refill the circulation during removal. The poor forward flow does not prove that adding volume will help. The next step is to identify whether the main limitation is cardiac function, vascular capacity, obstruction, or a combination.

19.2 Organ Flow Depends on Both Sides of the Pressure Gradient

Blood moves through a vascular bed because pressure is higher at its inlet than at its effective outlet. Vascular resistance determines how much flow that difference produces. A simple model expresses the relationship as:

Arterial inflow pressure is the pressure delivering blood to the organ. Effective outflow pressure is the downstream pressure that actually limits passage through its vessels. Resistance describes how strongly the vascular bed opposes flow. If pressures are in mm Hg and flow is in mL/min, the corresponding resistance unit is mm Hg·min/mL.

Start with an illustrative arterial pressure of 70 mm Hg and a relevant venous pressure of 8 mm Hg. The first value represents pressure entering the vascular bed. The second represents pressure opposing its drainage. Subtract the outlet value from the inlet value: 70 − 8 = 62 mm Hg. The model therefore gives a driving pressure of 62 mm Hg.

Now hold arterial pressure at 70 mm Hg and raise venous pressure to 20 mm Hg. The new difference is 70 − 20 = 50 mm Hg. The available pressure has fallen from 62 to 50 mm Hg because the downstream pressure rose. No fall in arterial pressure was needed to produce that change.

If resistance remained fixed, the smaller gradient would produce less flow. In a living organ, resistance can change through autoregulation, vasoconstriction, or vessel compression. Moreover, a central venous measurement may differ from the pressure at the organ's outlet. The subtraction therefore illustrates a mechanism; it does not measure the patient's organ blood flow or predict its exact reduction.

External pressure can alter the model further. A small vein surrounded by sufficiently high tissue pressure may narrow or collapse. Flow then depends on overcoming that local constraint. If tissue pressure or a vessel's closing pressure is the dominant limitation, central venous pressure is no longer the effective outlet pressure. Lowering an already lower central pressure may produce little additional flow.

Raising arterial pressure also changes more than the numerator. A vasopressor can increase arterial pressure while changing regional resistance and ventricular loading. Whether organ flow improves depends on the combined response. The equation supports examining both inflow and drainage; it does not support pursuing an indefinitely higher arterial pressure.

19.3 The Kidney Is Vulnerable to Impaired Venous Drainage

Renal venous hypertension affects the kidney through both its circulation and its tissue pressures. First, a higher renal venous pressure can reduce the pressure difference driving blood through the kidney. Second, pressure can rise within renal veins, capillaries, and the interstitium. The renal capsule limits how freely the swollen organ can expand, so additional tissue fluid can increase pressure within it.

These effects can interact. Increased interstitial pressure can compress small vessels and alter tubular pressures. Less blood may pass through some regions, and pressure within the tubules can oppose filtration upstream. The resulting change in filtration depends on the glomerular circulation, the tubular system, and the surrounding tissue together.

Glomerular filtration is distinct from renal blood flow. Filtration requires an appropriate pressure difference across the glomerular barrier, after accounting for opposing tubular and protein osmotic forces. A renal venous pressure rise cannot therefore be translated into one predictable change in glomerular pressure or filtration rate. It can change several pressures and resistances at once.

Winton's experiments in isolated mammalian kidneys showed that raising venous pressure could impair renal function under controlled conditions. They establish that venous conditions can directly affect the kidney. They do not define a central venous pressure above which every human kidney will fail. 1

Mullens and colleagues studied patients with advanced decompensated heart failure. Higher venous pressures were associated with worsening renal function, including across different cardiac-output measurements. This finding challenges an explanation based entirely on inadequate forward output. Because the study was observational, it cannot establish that venous pressure was the sole cause or that lowering it to one target would improve every patient's kidney function. 2

Congestion and other causes of kidney injury frequently coexist. A patient can have high renal venous pressure, reduced cardiac output, neurohormonal sodium retention, and inflammatory or toxic tubular injury. Identifying impaired drainage adds a mechanism to the assessment. It does not exclude ischemia, nephrotoxicity, urinary obstruction, or preexisting disease.

Oliguria alone consequently does not establish a need for more preload. Additional fluid may raise cardiac output when the circulation is responsive. If it mainly raises venous pressure, however, it can worsen the conditions for renal drainage without improving useful forward flow. Retained sodium and water can then aggravate the congestion that already limits excretion.

Assess the urine trajectory alongside cardiac function, arterial pressure, venous findings, recent fluid exposure, and alternative causes of injury. The question is how blood reaches and leaves the kidney, as well as what has happened within the kidney itself.

19.4 Central Venous Pressure Is a Contextual Measurement

Central venous pressure, or CVP, is usually measured near the right atrium relative to atmospheric pressure. It describes pressure at that location. The value results from the interaction of venous return, right-sided cardiac function, surrounding pressure, and measurement technique. It is not a direct measurement of total blood volume.

Before interpreting a change, establish that the measurement is credible. The pressure transducer must be zeroed and referenced to the appropriate level. Catheter position, waveform quality, and respiratory timing also matter. Moving the patient or transducer can change the displayed number without changing the circulation.

Next distinguish pressure inside the atrium from pressure across its wall. Transmural pressure is intracavitary pressure minus surrounding pressure. It is the pressure difference that distends the chamber. If intrathoracic pressure rises, the displayed CVP may rise even when the change in transmural pressure is much smaller.

Positive-pressure ventilation can produce this pattern, but its circulatory effects do not end with the pressure measurement. Lung inflation can increase right ventricular afterload. Increased thoracic pressure can impede venous return and change pressure transmission between the chest and abdomen. Cardiac output may fall, remain stable, or change for several simultaneous reasons. Assess those effects rather than dismissing the CVP rise as harmless or treating it automatically as added blood volume.

Legrand and colleagues found an association between higher CVP and new or persistent acute kidney injury in septic patients. Their retrospective analysis supports considering venous conditions during sepsis. It does not show that reducing CVP to a selected target prevents injury or that CVP captures every mechanism of septic kidney dysfunction. 3

A fluid challenge can reveal the relationship between pressure and forward flow. If CVP rises substantially while stroke volume changes little, the added volume has increased central pressure without a comparable gain in ejected blood. Examine right ventricular function, ventricular compliance, and organ congestion before repeating the infusion.

Baseline CVP still does not reliably predict fluid responsiveness. The same value can occur with different surrounding pressures, ventricular properties, and positions on the preload–stroke-volume curve. CVP becomes more informative when the waveform and trend are combined with the measured flow response and organ effects.

19.5 Congestion Has Different Regional Expressions

The systemic and pulmonary circulations connect through the heart, but congestion need not affect them equally. Increased left atrial pressure can raise pulmonary venous and microvascular pressures. Increased right atrial pressure can impede systemic venous drainage. The location of the cardiac limitation determines where pressure first accumulates.

Severe right ventricular failure can therefore produce jugular venous distension, hepatic congestion, and abdominal fluid accumulation without equally severe hydrostatic pulmonary edema. Acute left-sided dysfunction can produce pulmonary congestion before substantial dependent edema develops. Examining one side does not establish the pressure or fluid state of the other.

The liver drains through hepatic veins into the inferior vena cava near the right atrium. Increased downstream pressure can be transmitted into the hepatic veins and sinusoids. Sinusoidal distension and increased filtration contribute to hepatic enlargement and ascites. If cardiac output or arterial oxygen content also falls, reduced oxygen supply can add another form of injury.

Myers and colleagues examined clinical, hemodynamic, and histological findings in cardiac hepatopathy. Their study illustrates that cardiac disease can produce different hepatic abnormalities, with congestion and acute circulatory deterioration contributing in different ways. Liver-test abnormalities require interpretation in that setting, while also considering unrelated liver disease. 4

In the splanchnic circulation, impaired venous drainage can contribute to bowel-wall edema and abdominal fluid accumulation. As the contents of the abdomen expand, pressure may rise within the abdominal cavity. That pressure can further restrict venous drainage and affect the kidneys. The degree of pressure rise depends partly on how readily the abdominal wall and surrounding structures expand.

Peripheral edema has another set of influences. Gravity increases dependent venous pressures. Immobility reduces intermittent muscle compression that assists venous and lymphatic transport. Local venous disease, lymphatic function, and tissue compliance then shape the distribution of swelling. Leg edema does not directly quantify lung water or renal interstitial pressure.

Examine the neck veins, heart, lungs, abdomen, and dependent tissues as complementary sources of information. A missing physical sign may reflect a different regional distribution or an earlier stage of disease. A prominent sign in one region does not prove that every organ has the same abnormality.

19.6 External Pressure Can Worsen the Drainage Problem

A vessel's lumen depends partly on the pressure inside it relative to the pressure around it. When surrounding pressure rises, a thin-walled vein may narrow even without a fall in blood volume. This creates resistance to drainage. If compression is severe, the local external pressure may become the main pressure that blood must overcome.

Increased intra-abdominal pressure can act through this mechanism. It can compress abdominal veins and change the pressures around the kidneys. It also displaces the diaphragm and changes chest mechanics, linking an abdominal pressure problem to ventilation and cardiac loading.

The kidney may therefore face both increased renal venous pressure and increased surrounding tissue pressure. Subtracting thoracic CVP from mean arterial pressure does not fully represent either condition. A seemingly adequate central pressure difference can coexist with a local limitation to renal flow or filtration.

Mullens and colleagues studied intra-abdominal pressure in acute decompensated heart failure. They found relationships between abdominal pressure, renal dysfunction, and changes during treatment. These observations support examining the abdomen in cardiorenal assessment. They do not establish a universal decompressive intervention or require invasive pressure measurement in every patient with edema. 5

External pressure also affects measured filling pressures. An increase in displayed CVP may result partly from greater pressure around the right atrium. Alternatively, true atrial distension may increase, or both processes may occur together. Following a ventilator adjustment or new abdominal distension, interpret the pressure change with cardiac imaging and the response of forward flow.

Mechanical venous obstruction requires separate consideration. A thrombus or compressed major vein creates a local drainage problem that fluid removal alone may not resolve. Likewise, raising arterial pressure cannot be assumed to correct severe regional compression. The intervention must address the mechanism that actually limits flow.

The central question is where pressure opposes blood movement: within the draining vein, around a collapsible segment, or throughout a confined organ. Clinical assessment of intra-abdominal hypertension and compartment syndromes then requires standardized pressure measurement, accepted diagnostic definitions, and organ-specific management.

19.7 Venous Hypertension Promotes Edema Without Being Its Only Cause

Raised venous pressure can be transmitted upstream to the microcirculation. When capillary hydrostatic pressure rises, it favors movement of water out of the vascular compartment. How much pressure reaches the capillaries depends on the resistance between them and the venous outlet, as well as the region's vascular anatomy.

The amount of fluid that crosses the barrier also depends on permeability and protein-related osmotic forces. Inflammation can allow more fluid and protein to enter tissue. A pressure rise that produced little swelling before barrier injury can then generate a larger filtration load.

Lymphatic transport opposes accumulation by returning tissue fluid and protein to the circulation. Increased filtration may stimulate more lymph flow. Tissue fluid nevertheless continues to increase whenever entry exceeds removal. High lymph flow can therefore coexist with worsening edema if it remains insufficient for the incoming load.

Pressure and swelling also change on different time scales. An abrupt venous pressure rise can affect organ flow before visible edema develops. Once edema has accumulated, it takes time to clear even after vascular pressures fall. A pressure measurement describes current conditions, while swelling may partly reflect the preceding hours or days.

Venous hypertension is not the only cause of edema. Barrier injury, reduced protein-related opposition to filtration, local venous obstruction, and impaired lymphatic transport can contribute. Retained renal sodium and water can enlarge the fluid available to these processes. Several mechanisms commonly coexist in critical illness.

The word overloaded is therefore insufficient by itself. Specify whether the patient has retained fluid, increased venous pressure, impaired regional drainage, or tissue edema. These findings answer different questions and may require different responses.

The absence of dependent edema does not exclude congestion. Venous pressure may have risen recently, or its main consequences may be visceral. Conversely, persistent leg swelling does not prove that current cardiac filling pressures remain high or that additional removal will be tolerated. Interpret both pressure and tissue findings in their time course.

19.8 Venous Doppler Shows How Pulsations Reach an Organ

Venous Doppler measures the pattern of blood velocity through the cardiac and respiratory cycles. It shows when blood moves forward, slows, stops, or reverses at the sampled site. These changes provide information about pressure transmission and drainage. They do not directly measure total blood volume.

The inferior vena cava contributes central context. Its size and respiratory variation depend on right atrial conditions, surrounding pressure, spontaneous breathing effort, mechanical ventilation, and abdominal pressure. A dilated vena cava is therefore a finding to explain. It does not by itself specify an amount of fluid to remove.

The hepatic veins connect relatively directly with the right atrium. Changes in atrial pressure during the cardiac cycle influence their flow. Severe tricuspid regurgitation can send a strong systolic pressure wave backward, altering or reversing systolic hepatic venous flow. Rhythm and atrial function also affect the waveform.

The portal circulation is separated from the right atrium by the liver's vascular network. That network normally buffers much of the cardiac pulsation. Greater pressure transmission can make portal velocity more pulsatile, but liver disease and local vascular conditions alter the relationship. A portal waveform must therefore be interpreted in its hepatic context.

Within the kidney, changing downstream pressure and the surrounding tissue environment can interrupt venous flow during parts of the cardiac cycle. The waveform can become discontinuous rather than continuously forward. This is evidence about the conditions for drainage, not a direct measurement of glomerular filtration or proof of the only cause of kidney injury.

Iida and colleagues associated intrarenal venous Doppler patterns with right atrial pressure and outcomes in heart failure. More discontinuous patterns identified a different hemodynamic and prognostic state. This observational finding supports regional assessment. It does not show that treatment directed solely at normalizing the waveform improves kidney function. 6

Acquisition quality is essential. Confirm the vessel, sample position, Doppler settings, and relationship to the cardiac cycle. Document rhythm and breathing conditions. Compare serial recordings under similar conditions whenever possible, and interpret changes alongside cardiac findings and the clinical course.

19.9 VExUS Combines Findings but Does Not Replace Clinical Reasoning

The venous excess ultrasound approach, abbreviated VExUS, combines inferior vena cava assessment with hepatic, portal, and intrarenal venous Doppler. The rationale is that several concordant abnormalities provide stronger support for systemic venous congestion than one isolated finding. The individual waveforms remain important because they show where and how flow is disturbed.

Beaubien-Souligny and colleagues developed grading prototypes from repeated assessments in 145 cardiac surgical patients. The combination of a dilated vena cava and severe abnormalities in multiple Doppler beds was associated with subsequent acute kidney injury. This was a post-hoc analysis of a prospective cohort. It tested risk prediction, rather than a treatment strategy. 7

Risk prediction and treatment benefit answer different questions. An abnormal pattern may identify patients with more severe disease. That association does not establish which intervention will help, how rapidly fluid should be removed, or whether the pattern itself is causing the injury. Those questions require additional physiological assessment and intervention studies.

Islas-Rodríguez and colleagues randomized 140 patients with acute cardiorenal syndrome to VExUS-guided decongestion or usual clinical evaluation. Kidney function recovery, the primary endpoint, did not differ significantly. Measures of achieving decongestion favored the guided strategy, while reported 90-day survival was similar. This single-center trial provides treatment-guidance evidence in a defined population, without establishing improved kidney recovery or survival. 8

The study's scope matters when applying it to critical illness. Acute heart failure with worsening renal function is not identical to septic vasoplegia, severe acute respiratory distress syndrome, or obstructive right ventricular failure. The reasons for venous abnormalities and the consequences of fluid removal can differ across these settings.

A summary grade also compresses information. Similar grades can occur with different ventricular function, tricuspid regurgitation, rhythm, liver disease, or surrounding pressures. Review the images and the cardiac examination rather than allowing the grade to replace their interpretation.

VExUS can strengthen a congestion hypothesis and help follow its evolution. It cannot independently establish a safe removal rate or override worsening perfusion. A lower score is useful when it accompanies improvement in the patient's circulation and organ function; it is not by itself proof of a beneficial intervention.

19.10 Relieving Congestion Requires Attention to Perfusion and Refill

The treatment that relieves congestion depends on why venous pressure rose. Removing retained sodium and water can reduce venous filling. Improving right ventricular performance can help the heart move blood forward. Reducing excessive pulmonary vascular load or correcting mechanical obstruction addresses different limitations. Several approaches may be required in the same patient.

During fluid removal, water leaves the vascular compartment before all tissue edema has cleared. Tissue fluid must return to support plasma volume. As discussed in the preceding chapter, plasma refill is a changing net balance. A large amount of edema does not guarantee that fluid can return rapidly enough to match the current removal rate.

If vascular loss exceeds refill, cardiac filling and forward flow may fall. Arterial pressure can fall as well, although vasoconstriction may temporarily preserve it. Follow peripheral perfusion, cardiac performance, and organ responses alongside pressure. Stable blood pressure alone does not establish that the removal rate is tolerated.

Creatinine changes need their own interpretation. Serum creatinine is a concentration influenced by filtration, production, distribution, and time. During decongestion, a rise may reflect a functional reduction in filtration, concentration changes, structural injury, or several processes together. Magnitude, timing, urine findings, perfusion, and the overall trajectory help distinguish these possibilities.

In a CARRESS-HF biomarker substudy, Rao and colleagues examined patients with acute decompensated heart failure and preexisting worsening renal function. Further creatinine worsening during intensive volume removal was associated with increases in tubular injury markers. Marker increases also accompanied greater decongestion and better 60-day creatinine recovery. These observational associations within a selected trial cohort support interpreting filtration, marker changes, and later recovery separately. They do not establish that every creatinine rise is benign or justify continuing removal during worsening perfusion or another active renal insult. 9

The method of removal also matters. In CARRESS-HF, Bart and colleagues compared ultrafiltration with stepped pharmacological therapy in patients with decompensated heart failure, worsening renal function, and persistent congestion. The ultrafiltration strategy produced a less favorable creatinine response without superior weight loss and caused more serious adverse events. This result describes the tested strategy and population; it does not establish the effects of every individualized kidney-replacement prescription. 10

Judge decongestion by its combined effects. Falling venous pressure, less abnormal Doppler flow, and negative balance may support improvement when forward flow and organ perfusion remain adequate. The same measurements are less reassuring if the patient develops worsening peripheral perfusion, hypotension, or other evidence of circulatory deterioration.

The balance can change during treatment as vascular tone, cardiac loading, and refill evolve. Reassess rather than continuing solely to reach a normal-looking CVP, Doppler pattern, or fluid balance. The intended result is better organ conditions with sufficient circulation to sustain them.

19.11 Integrating a Congested Hemodynamic Pattern

Consider an illustrative ventilated patient with worsening oliguria and an increasingly positive fluid balance. Mean arterial pressure is 72 mm Hg. CVP is 18 mm Hg. Cardiac ultrasound shows a dilated, poorly functioning right ventricle, and regional venous Doppler shows marked abnormalities.

The arterial value represents pressure on the inflow side of the systemic circulation. CVP describes pressure near the right atrium on the drainage side. Subtracting the displayed central values gives 72 − 18 = 54 mm Hg. The arithmetic shows the difference between those two pressures. It is not a direct measurement of the kidney's perfusion pressure or blood flow.

The findings nevertheless form a coherent congestion hypothesis. The right ventricle is struggling to move blood forward, central venous pressure is elevated, and the regional waveforms suggest disturbed drainage. An arterial pressure of 72 mm Hg does not exclude these problems. The positive balance suggests fluid accumulation but does not establish how much of it can be removed safely at the present time.

Next identify what is limiting the right ventricle. Review pulmonary vascular load, oxygenation and ventilation, tricuspid valve function, rhythm, and surrounding pressures. Examine whether recent fluid administration increased stroke volume or mainly increased venous pressure. These observations distinguish an opportunity to improve forward flow from further filling that may aggravate congestion.

Assess other causes of oliguria in parallel. Sepsis-related injury, medications, urinary obstruction, and preexisting kidney disease remain possible. Low cardiac output and impaired venous drainage may coexist with intrinsic injury. No single congestion finding excludes the others.

Follow an intervention through both sides of the circulation. A higher arterial pressure without improved forward flow may leave the drainage problem unresolved. A lower CVP with worsening peripheral perfusion may indicate that vascular volume or cardiac support has become inadequate. Changes in ventilator settings or vasoactive treatment can alter these measurements simultaneously, so attribution requires attention to timing.

A favorable trajectory maintains or improves perfusion while reducing the relevant congestion. Evidence may include improved venous flow patterns, less respiratory impairment, a useful urine response, or gradual loss of tissue edema. These changes occur on different time scales and need not appear together.

The next chapter applies the same reasoning to fluid responsiveness and fluid tolerance. One assessment asks whether added preload will increase flow. The other asks whether the resulting pressures and fluid movement can be tolerated by vulnerable organs. A complete decision requires both.

References

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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(7):589–596. doi:10.1016/j.jacc.2008.05.068

3. Legrand M, Dupuis C, Simon C, et al. Association between systemic hemodynamics and septic acute kidney injury in critically ill patients: a retrospective observational study. Crit Care. 2013;17(6):R278. doi:10.1186/cc13133

4. Myers RP, Cerini R, Sayegh R, et al. Cardiac hepatopathy: clinical, hemodynamic, and histologic characteristics and correlations. Hepatology. 2003;37(2):393–400. doi:10.1053/jhep.2003.50062

5. Mullens W, Abrahams Z, Skouri HN, et al. Elevated intra-abdominal pressure in acute decompensated heart failure: a potential contributor to worsening renal function? J Am Coll Cardiol. 2008;51(3):300–306. doi:10.1016/j.jacc.2007.09.043

6. Iida N, Seo Y, Sai S, et al. Clinical implications of intrarenal hemodynamic evaluation by Doppler ultrasonography in heart failure. JACC Heart Fail. 2016;4(8):674–682. doi:10.1016/j.jchf.2016.03.016

7. 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. doi:10.1186/s13089-020-00163-w

8. Islas-Rodríguez JP, Miranda-Aquino T, Romero-González G, et al. Effect on kidney function recovery guiding decongestion with VExUS in patients with cardiorenal syndrome 1: a randomized control trial. Cardiorenal Med. 2024;14(1):1–11. doi:10.1159/000535641

9. Rao VS, Ahmad T, Brisco-Bacik MA, et al. Renal effects of intensive volume removal in heart failure patients with preexisting worsening renal function. Circ Heart Fail. 2019;12(6):e005552. doi:10.1161/CIRCHEARTFAILURE.118.005552

10. Bart BA, Goldsmith SR, Lee KL, et al. Ultrafiltration in decompensated heart failure with cardiorenal syndrome. N Engl J Med. 2012;367(24):2296–2304. doi:10.1056/NEJMoa1210357