Cardiorenal Med , DOI: 10.

1159/000534976
Received: June 22, 2023
Accepted: September 17, 2023
Published online: November 18, 2023

Downloaded from http://karger.com/crm/article-pdf/doi/10.1159/000534976/4049533/000534976.pdf by guest on 21 November 2023

Bedside Ultrasound in the Management of Cardiorenal Syndromes: An
Updated Review
Argaiz ER, Romero-Gonzalez G, Rola P, Spiegel R, Haycock KH, Koratala A

ISSN: 1664-3828 (Print), eISSN: 1664-5502 (Online)

https://www.karger.com/CRM
Cardiorenal Medicine

Disclaimer:
Accepted, unedited article not yet assigned to an issue. The statements, opinions and data contained in this
publication are solely those of the individual authors and contributors and not of the publisher and the editor(s). The
publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas,
methods, instructions or products referred to the content.

Copyright:
This article is licensed under the Creative Commons Attribution-NonCommercial 4.0 International License (CC BY-NC)
(http://www.karger.com/Services/OpenAccessLicense). Usage and distribution for commercial purposes requires
written permission.

© 2023 The Author(s). Published by S. Karger AG, Basel

Bedside Ultrasound in the Management of Cardiorenal Syndromes: An Updated Review

Authors:
Eduardo R Argaiz MD PhD1,2, Gregorio Romero-Gonzalez MD*3,4, Philippe Rola MD5, Rory Spiegel MD6, Korbin H
Haycock MD7,8, Abhilash Koratala MD9
1 Tecnologico de Monterrey, Escuela de Medicina y Ciencias de la Salud, Mexico
2 Nephrology Department, Instituto Nacional de Ciencias Médicas y Nutrición, Salvador Zubirán
3 Nephrology Department, University Hospital Germans Trias i Pujol, Badalona, Spain
4 International Renal Research Institute of Vicenza, Vicenza, Italia
5 Intensive Care Unit, Hopital Santa Cabrini Ospedale CEMTL, Montréal, QC, Canada
6 Department of Critical Care, Georgetown University Medstar Washington Hospital Center, Washington, DC, USA
7 Department of Emergency Medicine, Loma Linda University Health, Loma Linda, CA, USA
8 Department of Emergency Medicine, Riverside University Health System, Moreno Valley, CA, USA

Downloaded from http://karger.com/crm/article-pdf/doi/10.1159/000534976/4049533/000534976.pdf by guest on 21 November 2023

9 Division of Nephrology, Medical College of Wisconsin, Milwaukee, WI, USA
Running Title: POCUS in Cardiorenal Syndromes
*Corresponding Author: Gregorio Romero-Gonzalez.
garomerog.germanstrias@gencat.cat
Keywords: Cardiorenal syndrome, Venous Congestion, POCUS, VExUS, High Output Heart Failure

Abstract:
Background: Cardiorenal syndromes constitute a spectrum of disorders involving heart and kidney dysfunction
modulated by a complex interplay of neurohormonal, inflammatory and hemodynamic derangements. The
management of such patients often poses a diagnostic and therapeutic challenge to physicians owing to gaps in
understanding of pathophysiology, paucity of objective bedside diagnostic tools and individual biases. Summary: In
this narrative review, we discuss the role of clinician performed bedside ultrasound in the management of patients
with cardiorenal syndromes. Novel sonographic applications such as venous excess ultrasound (VExUS) are reviewed
in addition to lung and focused cardiac ultrasound. Further, underrecognized causes of heart failure such as high flow
arteriovenous fistula are discussed. Key Message: Bedside Ultrasound allows a comprehensive hemodynamic
characterization of cardiorenal syndromes.
Case
An 83-year-old woman was admitted with general deterioration and exertional dyspnea. She has a history of diabetes
mellitus, hypertension, and aortic valve replacement. She was found to have bilateral pleural effusions and acute
kidney injury with a serum creatinine of 2.04 mg/dl (baseline 1.1 mg/dl). Over the first few days following admission,
creatinine continued to rise. A formal echocardiogram showed normal biventricular contractility and mild mitral
stenosis. The treating team ascribed the worsening kidney function to diuretic therapy. Diuretics were held and
intravenous albumin was administered but the creatinine continued to rise to 3.44 mg/dl. In the following sections,
we will discuss the key aspects of evaluation and management of such cases before unwrapping further clinical
course.

Downloaded from http://karger.com/crm/article-pdf/doi/10.1159/000534976/4049533/000534976.pdf by guest on 21 November 2023

Introduction
There are a considerable number of neurohormonal, inflammatory and hemodynamic interactions between heart
failure and renal disease. Patients with chronic kidney disease lose the ability to adequately excrete excess dietary
sodium leading to volume overload, potentially exacerbating coexistent heart disease[1]. Similarly, chronic heart
failure can lead to acute or chronic kidney dysfunction predominantly mediated by backwards transmission of right
atrial pressure (RAP) to renal veins, venules and renal interstitium, a condition known as congestive nephropathy[2].
These different interactions led to the development of a classification system proposed by Ronco and colleagues[3]:
Cardiorenal syndromes refer to acute (Type 1) or chronic (Type 2) cardiac dysfunction leading to renal disease while
Renocardiac syndromes refer to acute kidney injury (Type 3) or chronic kidney disease (Type 4) leading to cardiac
dysfunction.
When managing these patients, it is now clear that achieving full decongestion, even if complicated by worsening
kidney function, is associated with improved short- and long-term outcomes[4]; However, excessive fluid removal or
failing to recognize significant cardiac dysfunction while decongesting can potentially lead to renal hypoperfusion and
tubular injury.
Clinicians caring for complex cardiorenal patients must possess the ability to perform comprehensive hemodynamic
evaluation and monitoring. Conventional physical examination lacks sensitivity and specificity for detecting residual
venous congestion and can suffers from reproducibility issues, even amongst experts[5,6]. Point-of-Care ultrasound
(POCUS) can enhance conventional physical examination in numerous ways including the detection of pulmonary and
systemic venous congestion, cardiac and valvular function and advanced hemodynamic monitoring including
pulmonary arterial pressures and estimation of pulmonary vascular resistance and cardiac output[7]. The correct
integration of clinical and ultrasonographic data can lead to individualized management tailored to unique
hemodynamic profiles of cardiorenal patients.
Cardiorenal Syndromes (Type 1 and 2)
Although many factors contribute to this interaction, hemodynamically significant venous congestion is one
of the most important mediators of renal dysfunction in heart failure. Using invasive hemodynamic measurements,
Mullens et al demonstrated that elevated central venous pressure (CVP) rather than decreased cardiac output is the
main driver of acute kidney injury (AKI) in patients with acute decompensated heart failure[8]. Congestion induced
acute renal dysfunction is mediated by the retrograde transmission of CVP to the kidneys leading to development of
interstitial edema and increased interstitial pressures. Because the kidneys are encapsulated organs, increased
interstitial pressure can result in global cessation of glomerular filtration, a condition known as intracapsular
tamponade (Fig. 1).
Chronically, venous congestion could have several detrimental consequences on renal function, although this has
been not explored in detail. Progressive decline in renal function has been observed in patients with chronic heart
failure[9]. Both decreased cardiac output and elevated CVP have been independently associated with low eGFR in
patients with pulmonary hypertension[10]. In animal models of experimental abdominal congestion, chronically
altered renal function has been observed[11]. In mice, congestion increases renal neutrophil adhesion and infiltration
which exacerbates kidney injury precipitated by a second hit[12]. Given the dominant role of venous congestion in
the development of the cardiorenal syndromes, it is conceivable that accurate assessment of RAP and the degree of
retrograde transmission to the abdominal organs play a pivotal role in appropriate management of these patients.
Furthermore, other strategies for evaluating venous congestion such as lung ultrasound (described later) should also
be assessed in these patients.
Bedside Ultrasound in Cardiorenal Syndromes
Ultrasound applications for evaluating venous congestion include inferior vena cava (IVC) size and collapsibility index
and internal jugular vein ultrasound. Given the IVC is a three-dimensional structure, evaluation in both long and short
axes is advised as this increases assessment accuracy[13]. Recently, a technique consisting of measuring the actual
depth of right atrium to calculate RAP using the internal jugular vein collapse point was shown to accurately estimate
RAP within 3 mm Hg as opposed to using an arbitrary distance of 5 cm[14].
It is important to understand that retrograde transmission of RAP to the abdominal organs depends not only on the
absolute CVP but also on the distensibility and volume of the peripheral veins. In venous congestion, maximally
stretched venous walls fail to accommodate retrograde flow and enhance pressure transmission to distal venules and

Downloaded from http://karger.com/crm/article-pdf/doi/10.1159/000534976/4049533/000534976.pdf by guest on 21 November 2023

capillary beds[15]. Consistent with this framework, experimental volume expansion in patients with heart failure has
been shown to increase renal congestion in the absence of noticeable changes in CVP[16]. In addition, in patients
heart failure, renal congestion has been shown to be the strongest predictor of adverse clinical outcomes
independently of CVP[17]. Therefore, bedside ultrasound estimation of CVP alone may not give adequate information
to guide management in cardiorenal syndrome; this is especially true in patients with right ventricular failure or
increased pulmonary vascular resistance where elevated CVP is found even in the compensated phase of the
disease[18]. Thus, not only the ability to assess RAP at the bedside, but also the degree of pressure transmission to
the kidneys and other abdominal organs provides a more complete hemodynamic information.
Doppler Evaluation of Organ Venous Congestion
Blood flow in the central veins (Inferior Vena Cava and Hepatic veins) is pulsatile in nature, this pulsatility is
related to pressure changes that occur with every cardiac cycle. In normal sinus rhythm, the normal sequence of
atrial contraction, atrial relaxation and ventricular relaxation are responsible for the normal “a” wave and “x” and “y”
descends of the CVP waveform respectively[19]. Doppler ultrasound of hepatic veins (HV) allows identification of 4
distinct waves which mirror the CVP waveform (A, S, V and D waves) (Fig. 2). When the transducer is placed along the
midaxillary line at the level of the liver, antegrade blood flow (from the liver to the heart) is plotted below the graph’s
baseline while retrograde flow (from the heart to the liver) appears above the baseline. The retrograde A wave occurs
during right atrial systole, while the antegrade S and D waves occur during right ventricular systole and diastole
respectively; normally, the S wave is larger in amplitude than the D wave (S > D pattern). Finally, the V wave is a
transitional retrograde wave occurring between S and D. While it is expected for the HV to be pulsatile, careful
analysis of the waveform pattern can provide useful information about the right heart function. Right ventricular
systolic dysfunction, moderate tricuspid regurgitation or elevated right ventricular end diastolic pressures can lead to
a decreased amplitude of the S wave, producing an S < D pattern. Severe tricuspid regurgitation will usually result in a
reverse S wave with retrograde flow. Increased pericardial pressure leads to impaired diastolic filling and D wave
reversal[20]. Simultaneous ECG and Doppler waveform acquisition is encouraged for accurate waveform
interpretation.
As opposed to flow in the HV, normal blood flow in the small venules and capillary beds of abdominal organs
is minimally pulsatile. Renal congestion can be evaluated by Doppler interrogation of flow in the small venules of the
kidney (interlobar or arcuate veins). Normal intra-renal venous flow (IRVF) is continuous or un-interrupted. In the
presence of venous congestion, IRVF becomes interrupted with interruptions becoming more prolonged as
congestion worsens. IRVF flow patterns were originally described by Iida et al in patients with chronic heart failure. In
this study, interrupted flow strongly correlated with adverse clinical outcomes independent of RAP or other heart
failure risk factors[17]. In patients with pulmonary hypertension, interrupted renal flow is associated with right heart
function, intra-abdominal pressure, hydration status, and independently predicts morbidity and mortality[21]. In
patients undergoing cardiac surgery, altered IRVF is an early indicator of acute congestion and a strong independent
predictor for the development of acute kidney injury[22]. In addition to interrupted IRVF patterns, milder intra-renal
flow alterations could represent a very sensitive marker of venous congestion which appear even before changes in
the IVC[16]. Increased IRVF pulsatility without flow interruptions is observed with experimental volume expansion in
patients with heart failure and this correlates with diuretic resistance[16]. In a recent cohort of ambulatory patients
with heart failure, 34% of patients with pulsatile IRVF had a normal IVC; However, in contrast to longer IRVF
interruptions, this milder pulsatile pattern was not significantly associated with adverse outcomes[23]. Given the
association between abnormal IRVD with right heart failure[17], focused cardiac ultrasound to assess right ventricular
function is suggested when altered IRVD is encountered.
Intra-renal Doppler can sometimes be technically challenging and time consuming[23]. Also, its interpretation
might not be reliable in patients with advanced chronic kidney disease, or hydronephrosis[24]. Doppler evaluation of
congestion at the level of the portal vein (PV) might provide an alternative site to evaluate pressure transmission to
distal capillary beds and, because of its larger size and better acoustic window, can be technically easier to perform.
PV doppler shows a high degree of agreement with IRVD and displays excellent reproducibility even among non-
expert sonographers[25]. Correct acquisition should be performed during and end-expiratory pause to avoid
respiratory variation. Similarly, to IRVF, normal PV flow is minimally pulsatile and becomes pulsatile with worsening
venous congestion. Increased PV pulsatility fraction has been associated with the development of congestive

Downloaded from http://karger.com/crm/article-pdf/doi/10.1159/000534976/4049533/000534976.pdf by guest on 21 November 2023

hepatopathy[26]. In cardiac surgery patients, increased PV pulsatility predicts acute kidney injury[22], congestive
encephalopathy[27] and intestinal edema[28]. There are important caveats to keep in mind when assessing portal
vein Doppler. In patients with advanced cirrhosis, PV flow can remain non-pulsatile even in the presence of severe
venous congestion[29]. On the other hand, arterio-portal shunts can present with increased portal vein pulsatility
even with normal heart function[30]. Also, Increased PV pulsatility has been described in healthy subjects with low
body mass index[31]. Given these limitations, a multi-organ congestion assessment score involving the IVC, HV, PV
and IRVF has been proposed (VExUS)(Fig. 3)[19]. This score was shown to be more specific for predicting AKI than any
of its individual components[32]. Recently, femoral vein Doppler has been proposed as easier site to evaluate
congestion displaying moderate agreement with the VExUS score[33].
Alterations of portal or intra-renal flows can be reversed after decongestive treatment. In patients with heart
failure, improvement to a non-interrupted IRVF was associated with a better prognosis even if baseline IRVF was
interrupted[34]. In patients with heart failure or pulmonary hypertension presenting with acute cardiorenal
syndrome, diuretic administration lead to normalization of PV flow and this coincided with AKI resolution[35]. A
recent study involving patients admitted to a cardiovascular ICU showed that increased PV pulsatility at baseline was
the best predictor of appropriate response to diuretics[36]. It is important to recognize that although hypervolemia
can worsen venous congestion, fluid removal is only one of many treatment options available. Depending on the
underlying cause of congestion, other strategies like pulmonary vasodilators[37], inotropes, vasodilators or even
arteriovenous fistula ligation[38] can better address this problem. The use of bedside ultrasound is not only
important in the initial assessment, but also in the subsequent management, as it can provide guidance to the
clinician when decongestive therapy has or has not achieved certain physiological goals. While these have not yet
been clearly established and warrant further study, the available data suggests that improving Doppler parameters
may improve outcomes. Figure 2 provides a pictorial summary of these Doppler patterns.
Evaluation of Low Cardiac Output States
While venous congestion is the main driver of renal dysfunction in patients with heart failure, significantly
decreased cardiac output jeopardizes renal perfusion. Hence, cardiac output estimation is an integral part of the
comprehensive hemodynamic assessment in patients with heart failure and oliguria or AKI[7]. Stroke volume can be
calculated by measuring the left ventricular outflow tract (LVOT) area in a parasternal long axis view of the heart and
multiplying it by the Velocity-time integral (VTI) of the flow obtained from apical 5-chamber view (Fig. 4)[39]. Because
of the large margin of error induced by the quadratic nature of the area formula, some authors recommend using the
LVOT VTI absolute value as a semi-quantitative estimation of stroke volume, with normal values being between 17-23
cm[39]. The finding of a significantly decreased cardiac output in the setting of acute cardiorenal syndrome should
prompt the search for hemodynamic interventions aimed at increasing stroke volume. In patients with severely
depressed left ventricular function, vasodilators or inodilators can reduce afterload and achieve this goal[40].
Fluid administration can sometimes improve cardiac output even in the presence of ventricular dysfunction.
When considering this strategy, it is important to first assess the potential harm of fluid administration. This risk
assessment is known as fluid tolerance evaluation[41]. In the absence of lung edema (determined by lung
ultrasound), severe systemic venous congestion (determined by venous Doppler) or abdominal compartment
syndrome (ascites with collapsed IVC), the patient can be considered fluid tolerant. After this, dynamic predictors of
fluid responsiveness can inform if fluid administration is likely to improve cardiac output. Cardiac output change
before and after passive leg rise is considered the gold standard for assessing fluid responsiveness[42].
Renocardiac Syndromes (Type 3 and 4)
Worsening cardiac function in patients with kidney disease is predominantly mediated by impaired sodium excretion
and volume overload. Other mechanisms including endothelial vascular calcification, calcific valvular disease,
inflammation, anemia and even the flow in the hemodialysis access also play a role[43]. In congested patients with
left heart failure and chronic kidney disease, achieving decongestion is associated with improved clinical outcomes
even in the setting worsening kidney function[44]. Creatinine elevation in the setting of decongestion is different
from “traditional AKI” as studies have shown negative biomarkers of tubular injury[45]. Because of this, decongestion
should still be attempted even if it leads to modest reductions in renal blood flow, a strategy that has also been
designed as “permissive AKI”[46].
Bedside Ultrasound in Renocardiac Syndromes

Downloaded from http://karger.com/crm/article-pdf/doi/10.1159/000534976/4049533/000534976.pdf by guest on 21 November 2023

Given the predominant role of chronic kidney disease induced volume overload in mediating heart failure
exacerbations, ultrasound assisted evaluation of the pulmonary status and systemic veins is a valuable tool in patients
with renocardiac syndromes. Detection of pulmonary congestion by lung ultrasound (LUS) is superior to classical
physical examination or chest radiography[47]. On LUS, pulmonary edema is represented by vertical, hyperechoic
ringdown artifacts known as B-lines (Fig. 5). In the presence of interstitial edema, micro-reflections at the sub-pleural
end are interpreted by the ultrasound machine as distance thus appearing on the screen as a narrow-based laser-like
ray. The presence of B-lines correlates well with elevated left ventricular end-diastolic pressure, and there is a strong
correlation between the change in pulmonary capillary wedge pressure and the number of B-lines on LUS[48].
Randomized control trials have consistently shown that LUS evaluation to follow up ambulatory patients with heart
failure leads to a significant reduction in urgent heart failure visits[49,50] or hospitalizations for acute
decompensated heart failure[51]. Various LUS scanning protocols have been described, including a 28-zone, an 8-
zone, a 6-zone, and a 4-zone approach (Fig. 6). Most studies aimed at detecting subclinical lung congestion have
utilized the comprehensive 28-zone protocol. However, recent research has shown that abbreviated protocols still
retain prognostic significance[52].
In patients with CKD undergoing hemodialysis (HD), LUS can detect real time improvement in lung edema
proportional to ultrafiltration volume[53]. Pre-dialysis B-line score is significantly associated with mortality
independently of bioimpedance-derived parameters[54]. In a largest cohort study, lung congestion detected by
ultrasound was independently associated with increased risk of mortality and cardiac events[55]. The LUST trial
randomized 367 patients on HD with a history of coronary artery disease or New York Heart Association (NYHA) class
III-IV heart failure to a LUS-guided intervention vs standard of care[56]. In this trial, increased B-Line count was
addressed mainly by lowering dry weight. While LUS-guided intervention did associate with lung congestion score
improvement, it did not result lower incidence of death, myocardial infarction, or de novo decompensated heart
failure. One possible explanation for this negative trial as proposed by the authors is that lung decongestion is a slow
process, as evidenced by the fact that reduction in long congestion reached its maximum near the end of the
intervention period. On a positive note, post hoc analysis of this trial did find significantly fewer recurrent episodes of
decompensated heart failure[56].
The evaluation of venous congestion has not been systematically studied in HD patients. In critically ill
patients undergoing HD, absence of venous congestion evaluated by IVC collapsibility index has been associated with
increased risk of intradialytic hypotension[57] and a lower likelihood of achieving the desired ultrafiltration goal[58].
Case reports of patients with severe pulmonary hypertension undergoing hemodialysis have shown rapid
improvement in portal vein flow pulsatility with ultrafiltration[38].
Figure 7 depicts some of the POCUS parameters that can be used to assess hemodynamics at the bedside. The key is
to recognize the continuity of hemodynamic circuit and avoid overreliance on isolated findings or measurements.
Arterio-Venous fistula and High Output Heart Failure
The prevalence of right ventricular dysfunction in patients with end-stage renal disease (ESRD) is significantly
higher in patients with an arterio-venous (AV) fistula HD access compared with those using a central venous catheter
or on peritoneal dialysis[59]. A prospective study found a prevalence of pulmonary hypertension of 39.7% in patients
receiving HD with a surgical AV access and in 0% of patients on peritoneal dialysis. In this study, patients with
increased pulmonary artery pressure also had significantly elevated cardiac output. Increased pulmonary artery
pressure is one of the hallmark hemodynamic derangements in high output heart failure (HOHF) along with increased
pulmonary wedge pressure and increased cardiac index (CI ≥ 4 l/min/m2)[60]. In the largest series reported, AV fistula
was the third most frequent cause of HOHF after obesity and cirrhosis[60]. In a large retrospective study, AV fistula
creation was associated with significant right ventricular dilatation and dysfunction, and this was independently
associated with increased mortality. Ligation of AV access led to decreased pulmonary artery pressures and 84% of
patients had stable or improving right ventricular function[61]. A clearly identified risk factor for the development of
AV access related HOHF is AV access flow, with flows > 2 l/min posing the greatest risk. A ratio of AV access blood
flow to cardiac output greater that 0.3 has also been shown to increase the risk[62].
The evaluation of the patient with heart failure and a large AV access can be greatly enhanced by POCUS.
Ultrasound performed at the bedside allows for the simultaneous estimation of access flow and cardiac output. AV
access flow is best estimated by measuring the mean velocity (cm/s) of the brachial artery which is then multiplied by

Downloaded from http://karger.com/crm/article-pdf/doi/10.1159/000534976/4049533/000534976.pdf by guest on 21 November 2023

the area of the vessel times 60 seconds[63]. Cardiac output can be estimated by measuring the LVOT diameter and
VTI[39], while the probability of pulmonary hypertension can be determined by measuring the velocity of the
tricuspid regurgitation jet[7]. Evaluation of venous congestion is also an integral part in the evaluation of HOHF and
can be performed using IVC ultrasound and venous Doppler[38]. While ultrasound evaluation can suggest the
underlying physiology of HOHF, invasive hemodynamic measurements are recommended in order to confirm this
diagnosis. In the setting of heart failure with pulmonary hypertension, increased AV fistula flow, high cardiac output
and persistent venous congestion despite attempts to lower dry weight, AV fistula flow reduction or fistula ligation
should be considered[64].
Case Continuation:
The POCUS team was consulted to assess volume status and possibly drain pleural effusions. The patient was found
to have moderate bilateral pleural effusions, moderate ascites, and a portal vein pulsatility over 100%. An increase in
diuretic dose was suggested but there was resistance from other consultants who had concerns about worsening of
the “pre-renal” state, as suggested by a low fractional excretion of sodium. The following day, after furosemide had
been increased, the creatinine was noted to be higher, at 3.92 mg/dl. The consulting nephrology and cardiology
services felt that this was an impasse and that continuing high dose furosemide was not indicated. Repeated POCUS
examination revealed significant congestion and, specifically, an interrupted monophasic pattern in the intrarenal
venous Doppler, suggesting that congestive nephropathy was likely a significant cause of worsening kidney function,
particularly in the absence of another potential culprit. Despite that, the treating physician opted to decrease the
diuretic dose. The following day, POCUS was repeated in the presence of consultants redemonstrating severe
congestion and a decision was made to administer intravenous furosemide. Over the next four days, the creatinine
decreased from to 1.8 mg/dl as she achieved a daily negative balance of 2L.
This case illustrates the understandable clinical difficulties in managing the cardiorenal patients, some of which can
be mitigated by POCUS showing the ongoing presence or absence of congestion as a potential factor in the worsening
kidney function. Figure 8 provides an algorithm incorporating POCUS in the management of AKI in patients with heart
failure.
Conclusions
POCUS allows a comprehensive hemodynamic evaluation of cardiorenal patients in both acute and
ambulatory settings. Given the relevance of venous congestion in the development of acute and possible chronic
renal dysfunction in heart failure patients, the quantification of organ congestion using venous Doppler is becoming
increasingly more relevant. This information, together with the evaluation of ventricular function, significant valvular
disease and hemodynamic parameters like cardiac output and pulmonary vascular resistance can help tailor
decongestive efforts to the individual physiology of every patient. In patients with chronic kidney disease and heart
failure, the evaluation of residual pulmonary congestion with LUS can inform on difficult situations like diuretic-
induced increase in serum creatinine. Finally, ultrasound-guided hemodynamic evaluation can suggest the possibility
of AV access indued heart failure in ESRD patients. Future studies should investigate how to best utilize various
POCUS applications to favorably impact the measurable outcomes.
Conflict of interest statement: Eduardo Argaiz: Speaker Honoraria from EchoNous. None of the authors have any
conflicts of interest to declare.
Funding Sources: No funding was used for this work.
Author Contributions: Eduardo R Argaiz wrote first draft and gave final approval, Gregorio Romero-Gonzalez critically
reviewed the manuscript and gave final approval, Philippe Rola conceptualized the original idea for the manuscript
and critically reviewed the manuscript, Rory Spiegel critically reviewed the manuscript, Korbin H Haycock critically
reviewed the manuscript, Abhilash Koratala critically reviewed the manuscript and gave final approval.
Data Availability Statement: No new data was generated for this manuscript
References:
1. Verbrugge FH, Dupont M, Steels P, Grieten L, Malbrain M, Tang WHW, et al. Abdominal Contributions to
Cardiorenal Dysfunction in Congestive Heart Failure. J Am Coll Cardiol. 2013 Aug;62(6):485–95.
2. Husain-Syed F, Gröne HJ, Assmus B, Bauer P, Gall H, Seeger W, et al. Congestive nephropathy: a neglected
entity? Proposal for diagnostic criteria and future perspectives. ESC Heart Fail. 2021 Feb;8(1):183–203.

Downloaded from http://karger.com/crm/article-pdf/doi/10.1159/000534976/4049533/000534976.pdf by guest on 21 November 2023

3. Ronco C, House AA, Haapio M. Cardiorenal and renocardiac syndromes: the need for a comprehensive
classification and consensus. Nat Clin Pract Nephrol. 2008 Jun;4(6):310–1.
4. Lucas C, Johnson W, Hamilton MA, Fonarow GC, Woo MA, Flavell CM, et al. Freedom from congestion
predicts good survival despite previous class IV symptoms of heart failure. Am Heart J. 2000 Dec;140(6):840–7.
5. Torino C, Gargani L, Sicari R, Letachowicz K, Ekart R, Fliser D, et al. The Agreement between Auscultation and
Lung Ultrasound in Hemodialysis Patients: The LUST Study. Clin J Am Soc Nephrol CJASN. 2016 Nov 7;11(11):2005–11.
6. Breidthardt T, Moreno-Weidmann Z, Uthoff H, Sabti Z, Aeppli S, Puelacher C, et al. How accurate is clinical
assessment of neck veins in the estimation of central venous pressure in acute heart failure? Insights from a
prospective study. Eur J Heart Fail. 2018;20(7):1160–2.
7. Koratala A, Kazory A. Point of Care Ultrasonography for Objective Assessment of Heart Failure: Integration of
Cardiac, Vascular, and Extravascular Determinants of Volume Status. Cardiorenal Med. 2021;11(1):5–17.
8. Mullens W, Abrahams Z, Francis GS, Sokos G, Taylor DO, Starling RC, et al. Importance of venous congestion
for worsening of renal function in advanced decompensated heart failure. J Am Coll Cardiol. 2009 Feb 17;53(7):589–
96.
9. Damman K, Masson S, Lucci D, Gorini M, Urso R, Maggioni AP, et al. Progression of Renal Impairment and
Chronic Kidney Disease in Chronic Heart Failure: An Analysis From GISSI-HF. J Card Fail. 2017 Jan;23(1):2–9.
10. Bitker L, Sens F, Payet C, Turquier S, Duclos A, Cottin V, et al. Presence of Kidney Disease as an Outcome
Predictor in Patients with Pulmonary Arterial Hypertension. Am J Nephrol. 2018;47(2):134–43.
11. Cops J, Mullens W, Verbrugge FH, Swennen Q, Reynders C, Penders J, et al. Selective abdominal venous
congestion to investigate cardiorenal interactions in a rat model. PLoS ONE. 2018 May 29;13(5):e0197687.
12. Kitani T, Kidokoro K, Nakata T, Kirita Y, Nakamura I, Nakai K, et al. Kidney vascular congestion exacerbates
acute kidney injury in mice. Kidney Int. 2022 Mar;101(3):551–62.
13. Seo Y, Iida N, Yamamoto M, Machino-Ohtsuka T, Ishizu T, Aonuma K. Estimation of Central Venous Pressure
Using the Ratio of Short to Long Diameter from Cross-Sectional Images of the Inferior Vena Cava. J Am Soc
Echocardiogr Off Publ Am Soc Echocardiogr. 2017 May;30(5):461–7.
14. Istrail L, Kiernan J, Stepanova M. A novel method for estimating right atrial pressure with point-of-care
ultrasound. J Am Soc Echocardiogr (Internet). 2022 Dec 12 (cited 2023 Jan 2);0(0). Available from:
https://www.onlinejase.com/article/S0894-7317(22)00650-2/fulltext
15. Argaiz ER. VExUS Nexus: Bedside Assessment of Venous Congestion. Adv Chronic Kidney Dis. 2021
May;28(3):252–61.
16. Nijst P, Martens P, Dupont M, Tang WHW, Mullens W. Intrarenal Flow Alterations During Transition From
Euvolemia to Intravascular Volume Expansion in Heart Failure Patients. JACC Heart Fail. 2017;5(9):672–81.
17. Iida N, Seo Y, Sai S, Machino-Ohtsuka T, Yamamoto M, Ishizu T, et al. Clinical Implications of Intrarenal
Hemodynamic Evaluation by Doppler Ultrasonography in Heart Failure. JACC Heart Fail. 2016;4(8):674–82.
18. Via G, Tavazzi G, Price S. Ten situations where inferior vena cava ultrasound may fail to accurately predict
fluid responsiveness: a physiologically based point of view. Intensive Care Med. 2016 Jul 1;42(7):1164–7.
19. Rola P, Miralles-Aguiar F, Argaiz E, Beaubien-Souligny W, Haycock K, Karimov T, et al. Clinical applications of
the venous excess ultrasound (VExUS) score: conceptual review and case series. Ultrasound J. 2021 Jun 19;13(1):32.
20. Reynolds T, Appleton CP. Doppler flow velocity patterns of the superior vena cava, inferior vena cava, hepatic
vein, coronary sinus, and atrial septal defect: a guide for the echocardiographer. J Am Soc Echocardiogr Off Publ Am
Soc Echocardiogr. 1991 Oct;4(5):503–12.
21. Husain-Syed F, Birk HW, Ronco C, Schörmann T, Tello K, Richter MJ, et al. Doppler-Derived Renal Venous
Stasis Index in the Prognosis of Right Heart Failure. J Am Heart Assoc. 2019 Nov 5;8(21):e013584.
22. Beaubien-Souligny W, Benkreira A, Robillard P, Bouabdallaoui N, Chassé M, Desjardins G, et al. Alterations in
Portal Vein Flow and Intrarenal Venous Flow Are Associated With Acute Kidney Injury After Cardiac Surgery: A
Prospective Observational Cohort Study. J Am Heart Assoc. 2018 02;7(19):e009961.
23. Pugliese NR, Pellicori P, Filidei F, Del Punta L, De Biase N, Balletti A, et al. The incremental value of multi-
organ assessment of congestion using ultrasound in outpatients with heart failure. Eur Heart J - Cardiovasc Imaging.
2023 Jan 3;jeac254.

Downloaded from http://karger.com/crm/article-pdf/doi/10.1159/000534976/4049533/000534976.pdf by guest on 21 November 2023

24. Koratala A, Reisinger N. Venous Excess Doppler Ultrasound for the Nephrologist: Pearls and Pitfalls. Kidney
Med (Internet). 2022 Jul 1 (cited 2023 Jan 2);4(7). Available from:
https://www.kidneymedicinejournal.org/article/S2590-0595(22)00098-X/fulltext
25. Gómez-Rodríguez C, Tadeo-Espinoza H, Solis-Huerta F, Leal-Villarreal MADJ, Guerrero-Cabrera P, Cruz N, et al.
Hemodynamic Evaluation of Right-Sided Congestion With Doppler Ultrasonography in Pulmonary Hypertension. Am J
Cardiol. 2023 Sep;203:459–62.
26. Styczynski G, Milewska A, Marczewska M, Sobieraj P, Sobczynska M, Dabrowski M, et al. Echocardiographic
Correlates of Abnormal Liver Tests in Patients with Exacerbation of Chronic Heart Failure. J Am Soc Echocardiogr Off
Publ Am Soc Echocardiogr. 2016 Feb;29(2):132–9.
27. Benkreira A, Beaubien-Souligny W, Mailhot T, Bouabdallaoui N, Robillard P, Desjardins G, et al. Portal
Hypertension Is Associated With Congestive Encephalopathy and Delirium After Cardiac Surgery. Can J Cardiol.
2019;35(9):1134–41.
28. Ikeda Y, Ishii S, Yazaki M, Fujita T, Iida Y, Kaida T, et al. Portal congestion and intestinal edema in hospitalized
patients with heart failure. Heart Vessels. 2018 Jul 1;33(7):740–51.
29. Loperfido F, Lombardo A, Amico CM, Vigna C, Testa M, Rossi E, et al. Doppler analysis of portal vein flow in
tricuspid regurgitation. J Heart Valve Dis. 1993 Mar;2(2):174–82.
30. Gorka W, Gorka TS, Lewall DB. Doppler ultrasound evaluation of advanced portal vein pulsatility in patients
with normal echocardiograms. Eur J Ultrasound. 1998 Nov;8(2):119–23.
31. Gallix BP, Taourel P, Dauzat M, Bruel JM, Lafortune M. Flow pulsatility in the portal venous system: a study of
Doppler sonography in healthy adults. AJR Am J Roentgenol. 1997 Jul;169(1):141–4.
32. Beaubien-Souligny W, Rola P, Haycock K, Bouchard J, Lamarche Y, Spiegel R, et al. Quantifying systemic
congestion with Point-Of-Care ultrasound: development of the venous excess ultrasound grading system. Ultrasound
J (Internet). 2020 Apr 9 (cited 2020 May 5);12. Available from:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7142196/
33. Bhardwaj V, Rola P, Denault A, Vikneswaran G, Spiegel R. Femoral vein pulsatility: a simple tool for venous
congestion assessment. Ultrasound J. 2023 May 10;15:24.
34. Yamamoto M, Seo Y, Iida N, Ishizu T, Yamada Y, Nakatsukasa T, et al. Prognostic Impact of Changes in
Intrarenal Venous Flow Pattern in Patients With Heart Failure. J Card Fail. 2021 Jan;27(1):20–8.
35. Argaiz ER, Rola P, Gamba G. Dynamic Changes in Portal Vein Flow during Decongestion in Patients with Heart
Failure and Cardio-Renal Syndrome: A POCUS Case Series. Cardiorenal Med. 2021;11(1):59–66.
36. Guinot PG, Bahr PA, Andrei S, Popescu BA, Caruso V, Mertes PM, et al. Doppler study of portal vein and renal
venous velocity predict the appropriate fluid response to diuretic in ICU: a prospective observational
echocardiographic evaluation. Crit Care. 2022 Oct 5;26(1):305.
37. Elmi-Sarabi M, Jarry S, Couture EJ, Haddad F, Cogan J, Sweatt AJ, et al. Pulmonary Vasodilator Response of
Combined Inhaled Epoprostenol and Inhaled Milrinone in Cardiac Surgical Patients. Anesth Analg. 2022 Oct
2;10.1213/ANE.0000000000006192.
38. Argaiz ER, Cruz N, Gamba G. Evaluation of rapid changes in haemodynamic status by Point-of-Care
Ultrasound: a useful tool in cardionephrology. Clin Kidney J. 2022 Feb;15(2):360–2.
39. Blanco P. Rationale for using the velocity-time integral and the minute distance for assessing the stroke
volume and cardiac output in point-of-care settings. Ultrasound J. 2020 Apr 21;12(1):21.
40. Verbrugge FH, Grieten L, Mullens W. Management of the cardiorenal syndrome in decompensated heart
failure. Cardiorenal Med. 2014 Dec;4(3–4):176–88.
41. Argaiz ER, Rola P, Haycock KH, Verbrugge FH. Fluid management in acute kidney injury: from evaluating fluid
responsiveness towards assessment of fluid tolerance. Eur Heart J Acute Cardiovasc Care. 2022 Nov 2;11(10):786–93.
42. Monnet X, Cipriani F, Camous L, Sentenac P, Dres M, Krastinova E, et al. The passive leg raising test to guide
fluid removal in critically ill patients. Ann Intensive Care. 2016 May 20;6:46.
43. Banerjee D, Rosano G, Herzog CA. Management of Heart Failure Patient with CKD. Clin J Am Soc Nephrol
CJASN. 2021 Jul;16(7):1131–9.
44. Kazory A. The Congestion-Creatinine Interplay in Acute Heart Failure: Time to Move Up to the Next Level. Am

Downloaded from http://karger.com/crm/article-pdf/doi/10.1159/000534976/4049533/000534976.pdf by guest on 21 November 2023

J Med. 2020 Mar;133(3):259–60.
45. Ahmad T, Jackson K, Rao VS, Tang WHW, Brisco-Bacik MA, Chen HH, et al. Worsening Renal Function in
Patients With Acute Heart Failure Undergoing Aggressive Diuresis Is Not Associated With Tubular Injury. Circulation.
2018 May 8;137(19):2016–28.
46. Parikh CR, Coca SG. “Permissive AKI” with treatment of heart failure. Kidney Int. 2019 Nov 1;96(5):1066–8.
47. Maw AM, Hassanin A, Ho PM, McInnes MDF, Moss A, Juarez-Colunga E, et al. Diagnostic Accuracy of Point-of-
Care Lung Ultrasonography and Chest Radiography in Adults With Symptoms Suggestive of Acute Decompensated
Heart Failure: A Systematic Review and Meta-analysis. JAMA Netw Open. 2019 Mar 1;2(3):e190703.
48. Rivas-Lasarte M, Solé-González E, Álvarez-García J, Maestro A, Garcia-Picart J, Roig E, et al. Dynamic
Correlation Between Cardiac Filling Pressures and B-Lines in a Lung Ultrasound: A Pilot Study. J Card Fail. 2021
Mar;27(3):379–81.
49. Rivas-Lasarte M, Álvarez-García J, Fernández-Martínez J, Maestro A, López-López L, Solé-González E, et al.
Lung ultrasound-guided treatment in ambulatory patients with heart failure: a randomized controlled clinical trial
(LUS-HF study). Eur J Heart Fail. 2019;21(12):1605–13.
50. Araiza-Garaygordobil D, Gopar-Nieto R, Martinez-Amezcua P, Cabello-López A, Alanis-Estrada G, Luna-Herbert
A, et al. A randomized controlled trial of lung ultrasound guided therapy in heart failure (CLUSTER-HF study). Am
Heart J (Internet). 2020 Jun 15 (cited 2020 Jul 2); Available from:
http://www.sciencedirect.com/science/article/pii/S0002870320301836
51. Marini C, Fragasso G, Italia L, Sisakian H, Tufaro V, Ingallina G, et al. Lung ultrasound-guided therapy reduces
acute decompensation events in chronic heart failure. Heart Br Card Soc. 2020 Dec 1;106(24):1934–9.
52. Reisinger N, Lohani S, Hagemeier J, Panebianco N, Baston C. Lung Ultrasound to Diagnose Pulmonary
Congestion Among Patients on Hemodialysis: Comparison of Full Versus Abbreviated Scanning Protocols. Am J Kidney
Dis Off J Natl Kidney Found. 2022 Feb;79(2):193-201.e1.
53. Noble VE, Murray AF, Capp R, Sylvia-Reardon MH, Steele DJR, Liteplo A. Ultrasound assessment for
extravascular lung water in patients undergoing hemodialysis. Time course for resolution. Chest. 2009
Jun;135(6):1433–9.
54. Siriopol D, Hogas S, Voroneanu L, Onofriescu M, Apetrii M, Oleniuc M, et al. Predicting mortality in
haemodialysis patients: a comparison between lung ultrasonography, bioimpedance data and echocardiography
parameters. Nephrol Dial Transplant Off Publ Eur Dial Transpl Assoc - Eur Ren Assoc. 2013 Nov;28(11):2851–9.
55. Zoccali C, Torino C, Tripepi R, Tripepi G, D’Arrigo G, Postorino M, et al. Pulmonary congestion predicts cardiac
events and mortality in ESRD. J Am Soc Nephrol JASN. 2013 Mar;24(4):639–46.
56. Zoccali C, Torino C, Mallamaci F, Sarafidis P, Papagianni A, Ekart R, et al. A randomized multicenter trial on a
lung ultrasound–guided treatment strategy in patients on chronic hemodialysis with high cardiovascular risk. Kidney
Int. 2021 Dec 1;100(6):1325–33.
57. da Hora Passos R, Caldas J, Ramos JGR, dos Santos Galvão de Melo EB, Ribeiro MPD, Alves MFC, et al.
Ultrasound-based clinical profiles for predicting the risk of intradialytic hypotension in critically ill patients on
intermittent dialysis: a prospective observational study. Crit Care. 2019 Dec 2;23(1):389.
58. Kaptein MJ, Kaptein JS, Oo Z, Kaptein EM. Relationship of inferior vena cava collapsibility to ultrafiltration
volume achieved in critically ill hemodialysis patients. Int J Nephrol Renov Dis. 2018;11:195–209.
59. Paneni F, Gregori M, Ciavarella GM, Sciarretta S, De Biase L, Marino L, et al. Right ventricular dysfunction in
patients with end-stage renal disease. Am J Nephrol. 2010;32(5):432–8.
60. Reddy YNV, Melenovsky V, Redfield MM, Nishimura RA, Borlaug BA. High-Output Heart Failure: A 15-Year
Experience. J Am Coll Cardiol. 2016 Aug 2;68(5):473–82.
61. Reddy YNV, Obokata M, Dean PG, Melenovsky V, Nath KA, Borlaug BA. Long-term cardiovascular changes
following creation of arteriovenous fistula in patients with end stage renal disease. Eur Heart J. 2017 Jun
21;38(24):1913–23.
62. Wijnen E, Keuter XH, Planken NR, van der Sande FM, Tordoir JH, Leunissen KM, et al. The relation between
vascular access flow and different types of vascular access with systemic hemodynamics in hemodialysis patients.
Artif Organs. 2005 Dec;29(12):960–4.
63. Voiculescu AS, Hentschel DM. Point-of-care Vascular Ultrasound: Of Fistulas and Flows. Adv Chronic Kidney

Downloaded from http://karger.com/crm/article-pdf/doi/10.1159/000534976/4049533/000534976.pdf by guest on 21 November 2023

Dis. 2021 May;28(3):227–35.
64. Clarkson MR, Giblin L, Brown A, Little D, Donohoe J. Reversal of pulmonary hypertension after ligation of a
brachiocephalic arteriovenous fistula. Am J Kidney Dis. 2002 Sep 1;40(3):e8.1-e8.4.
Figure legends:

Fig. 1: Summary of congestive nephropathy: Congestion induced acute renal dysfunction is mediated by retrograde
transmission of central venous pressure to the kidneys leading to development of interstitial edema, inflammation,
and activation of the renin angiotensin aldosterone system (RAAS) and sympathetic nervous system (SNS). This
further results in global cessation of glomerular filtration. Intraabdominal hypertension adds to the problem by
simulating a tamponade pathophysiology together with increased interstitial pressures.

Fig. 2: Sonographic markers of venous congestion: Left panel represents normal right ventricle (RV), right atrial
pressure (RAP) as suggested by a nondilated inferior vena cava (IVC) and normal venous Doppler waveforms. Right
panel depicts a dilated RV with tricuspid regurgitation (TR), a plethoric IVC indicative of elevated RAP and transition of
venous Doppler waveforms with worsening congestion. S = systolic wave, D = diastolic wave.

Downloaded from http://karger.com/crm/article-pdf/doi/10.1159/000534976/4049533/000534976.pdf by guest on 21 November 2023

Fig. 3: Venous Excess Ultrasound Score (VExUS) grading.

Fig. 4: Estimation of stroke volume and cardiac output on focused cardiac ultrasound. LV = left ventricle, Ao = aorta.
Figure made using Biorender®

Fig. 5: Lung ultrasound findings: horizontal A-lines (normal) and vertical B-lines (abnormal).

Fig. 6: Lung ultrasound protocols including the 28-zone (upper left panel), 8-zone (upper right panel), a 6- and 4-zone
approach (lower left panel). An example of real-life lung ultrasound report is presented in lower right panel, 8-zone
approach is used with 4 right zones (R 1-4) and 4 left zones (L 1-4). The number of B-Lines in each zone is included in
the report.

Fig. 7: Summary of point-of-care ultrasound parameters that can be used in the assessment of hemodynamics.
Normal sonographic images shown for illustration purposes.
IJ, internal jugular; RAP, right atrial pressure; TR, tricuspid regurgitation; IVC, inferior vena cava; US, ultrasound;
VExUS, venous excess ultrasound; LV, left ventricular; LVOT, left ventricular outflow tract.
Figure reused from Koratala, et al., doi: 10.34067/KID.0005522022 with kind permission of the publisher.

Fig. 8: Algorithm incorporating POCUS in the management of AKI in patients with heart failure. AHF, acute heart
failure; JVP, jugular venous pulse; LUS, lung ultrasound; IVC, inferior vena cava; AKI, acute kidney injury; SI-AKI, sepsis-
induced AKI; ATN, acute tubular necrosis; AIN, acute interstitial nephritis; UNa, urine sodium; LVOT-VTI; left
ventricular outflow tract – velocity time integral; CRT, capillary refill time; LV, left ventricular; RV right ventricular; CO,
cardiac output; RAAS, renin angiotensin aldosterone system; d/c, discontinue.
Downloaded from http://karger.com/crm/article-pdf/doi/10.1159/000534976/4049533/000534976.pdf by guest on 21 November 2023
Downloaded from http://karger.com/crm/article-pdf/doi/10.1159/000534976/4049533/000534976.pdf by guest on 21 November 2023
Downloaded from http://karger.com/crm/article-pdf/doi/10.1159/000534976/4049533/000534976.pdf by guest on 21 November 2023
Downloaded from http://karger.com/crm/article-pdf/doi/10.1159/000534976/4049533/000534976.pdf by guest on 21 November 2023
Downloaded from http://karger.com/crm/article-pdf/doi/10.1159/000534976/4049533/000534976.pdf by guest on 21 November 2023
Downloaded from http://karger.com/crm/article-pdf/doi/10.1159/000534976/4049533/000534976.pdf by guest on 21 November 2023
Downloaded from http://karger.com/crm/article-pdf/doi/10.1159/000534976/4049533/000534976.pdf by guest on 21 November 2023
Downloaded from http://karger.com/crm/article-pdf/doi/10.1159/000534976/4049533/000534976.pdf by guest on 21 November 2023