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 who performed bedside ultrasound in the management of patients with cardiorenal syndromes. Novel sonographic applications such as venous excess ultrasound score (VExUS) are reviewed in addition to the 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.

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.

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 backward 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 (AKI) (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 suffer from reproducibility issues, even among 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.

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. [8] demonstrated that elevated central venous pressure (CVP) rather than decreased cardiac output is the main driver of AKI in patients with acute decompensated heart failure. 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).

Fig. 1.

Summary of congestive nephropathy: congestion-induced acute renal dysfunction is mediated by retrograde transmission of CVP 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. Intra-abdominal hypertension adds to the problem by simulating a tamponade pathophysiology together with increased interstitial pressures.

Fig. 1.

Summary of congestive nephropathy: congestion-induced acute renal dysfunction is mediated by retrograde transmission of CVP 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. Intra-abdominal hypertension adds to the problem by simulating a tamponade pathophysiology together with increased interstitial pressures.

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Chronically, venous congestion could have several detrimental consequences on renal function, although this has not been 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 (LUS) (described later) should also be assessed in these patients.

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 the 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 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 (IVC and hepatic veins [HV]) 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 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.

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.

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.

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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 intrarenal venous flow (IRVF) is continuous or uninterrupted. 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. [17] 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. 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 AKI [22]. In addition to interrupted IRVF patterns, milder intrarenal 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.

Intrarenal 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 hepatopathy [26]. In cardiac surgery patients, increased PV pulsatility predicts AKI [22], congestive encephalopathy [27], and intestinal edema [28]. There are important caveats to keep in mind when assessing PV 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 PV 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].

Fig. 3.

Venous Excess Ultrasound Score (VExUS) grading.

Fig. 3.

Venous Excess Ultrasound Score (VExUS) grading.

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Alterations of portal or intrarenal 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 (AV) 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 suggest 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 semiquantitative estimation of stroke volume, with normal values being between 17 and 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].

Fig. 4.

Estimation of stroke volume and cardiac output on focused cardiac ultrasound. LV, left ventricle; Ao, aorta (figure made using Biorender®).

Fig. 4.

Estimation of stroke volume and cardiac output on focused cardiac ultrasound. LV, left ventricle; Ao, aorta (figure made using Biorender®).

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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 LUS), 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].

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 (HD) 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].

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 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 subpleural 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].

Fig. 5.

LUS findings: horizontal A-lines (normal) and vertical B-lines (abnormal).

Fig. 5.

LUS findings: horizontal A-lines (normal) and vertical B-lines (abnormal).

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Fig. 6.

LUS 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 LUS report is presented in lower right panel, and 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. 6.

LUS 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 LUS report is presented in lower right panel, and 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.

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In patients with CKD undergoing HD, LUS can detect real-time improvement in lung edema proportional to ultrafiltration volume [53]. Predialysis 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 versus 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 HD have shown rapid improvement in PV 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.

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 score; 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. 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 score; 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).

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AV Fistula and High-Output Heart Failure

The prevalence of right ventricular dysfunction in patients with end-stage renal disease is significantly higher in patients with an 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 than 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 the area of the vessel times 60 s [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].

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 PV pulsatility over 100%. An increase in diuretic dose was suggested, but there was resistance from other consultants who had concerns about worsening of the “prerenal” 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 4 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.

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.

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.

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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-induced heart failure in end-stage renal disease patients. Future studies should investigate how to best utilize various POCUS applications to favorably impact the measurable outcomes.

Eduardo Argaiz has received speaker honoraria from EchoNous. Other authors do not have any conflicts of interest to declare.

No funding was used for this work.

Eduardo R. Argaiz wrote the first draft and gave the final approval. Gregorio Romero-Gonzalez critically reviewed the manuscript and gave the 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 the final approval.

No new data were generated for this manuscript.

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