Evaluation and management of heart failure caused by hemodialysis arteriovenous access

INTRODUCTION — Creation of a hemodialysis arteriovenous (AV) access (via constructed native AV fistula or a prosthetic AV graft) causes an acute decrease in systemic vascular resistance and a secondary increase in cardiac output [1,2]. The increased cardiac output is usually clinically insignificant but may rarely result in overt heart failure, particularly among patients with underlying heart disease. (See 'Pathogenesis' below.)

The pathogenesis, diagnosis, and management of hemodialysis AV access causing or exacerbating heart failure are presented in this topic review. High-output heart failure and the effects of hemodialysis AV access on pulmonary hypertension are discussed elsewhere. (See "Causes and pathophysiology of high-output heart failure" and "Pulmonary hypertension in patients with end-stage kidney disease".)

A general discussion of myocardial dysfunction in the patient with end-stage kidney disease (ESKD) is presented separately. (See "Overview of screening and diagnosis of heart disease in patients on dialysis".)

EPIDEMIOLOGY AND RISK FACTORS — Heart failure and chronic kidney disease (CKD) are increasingly concurrent, especially in older patients and patients with hypertension, diabetes, or other cardiovascular comorbidities [3]. With the development of end-stage kidney disease (ESKD), the hemodynamic effects of a functioning hemodialysis arteriovenous (AV) access creates an additional burden on cardiac function and can cause or exacerbate heart failure [1]. Although the development of heart failure from the hemodynamic demands of hemodialysis AV access is predominantly limited to patients who have preexisting cardiovascular disease and/or cardiovascular risk factors, most patients on hemodialysis have cardiovascular disease or such risk factors. (See "Risk factors and epidemiology of coronary heart disease in end-stage kidney disease (dialysis)".)

Heart failure is common among patients on hemodialysis; estimates of heart failure prevalence vary in this population but range between 30 and 70 percent [4-8]. However, limited data are available on the risk of hemodialysis access worsening or precipitating heart failure [9-15]:

●In a prospective study involving 562 patients with CKD who had estimated glomerular filtration rate (eGFR) 30 to 59 mL/min/1.73 m², 17 percent developed at least one episode of predialysis heart failure [16]. Among these patients, risk factors for acute heart failure included traditional risk factors (eg, diabetes, coronary artery disease, and prior history of heart failure) as well as the presence of functioning hemodialysis AV access [16].

●In a retrospective study of 113 kidney transplant recipients who had previously undergone hemodialysis via hemodialysis AV access, 25.7 percent required hemodialysis AV access closure, primarily because of symptoms of heart failure [17]. The mean shunt flow among patients treated with shunt closure was 2197 mL/min compared with 851 mL/min among patients who did not undergo shunt closure.

●In a prospective study of 214 patients on hemodialysis in which 122 (57 percent) were diagnosed with heart failure, 19 (9 percent) had high-output heart failure (defined by heart failure signs and symptoms plus a cardiac index >3.9 L/min/m²); among these 19 patients, heart failure was attributed directly to high hemodialysis AV access flows in 11 (60 percent) [8].

Factors associated with hemodialysis AV access precipitating heart failure include development of right ventricular (RV) dilatation, left atrial dilation, development of atrial fibrillation, male sex, prior vascular access surgery, and high hemodialysis AV access flow rate (Qa) [1]. The risk of worsening heart failure is directly proportional to the flow of the hemodialysis AV access and is greater with worse pre-existing cardiac function [18]. There is no threshold Qa that defines risk. Even what is considered to be a normal flow may worsen or precipitate heart failure in patients with pre-existing heart failure or heart disease.

Similar rates of heart failure have been observed among patients with AV fistulas compared with those with AV grafts [1,19]. For AV fistulas, the risk of precipitating heart failure appears to be higher among patients who have an upper-arm AV fistula compared with forearm AV fistula [11,16,17,20]. The higher risk associated with upper-arm AV fistulas appears to be related to higher blood flow [21]. In a study including 96 patients with AV fistulas, 10 developed high-output cardiac failure after the AV fistula was placed [11].

Significantly higher blood flow rates were seen in the upper-arm versus the forearm AV fistulas (1.58 versus 0.948 L/min) [11]. In the above cited observational study of 562 predialysis patients, the incidence of heart failure was much higher in patients who had a brachiocephalic AV fistula compared with those with a radial-cephalic AV fistula (40 versus 8 percent) [16].

Changes in flow over time in response to an AV access are discussed below. (See 'Subacute and chronic changes' below.)

PATHOGENESIS — The creation of a hemodialysis arteriovenous (AV) access results in acute, subacute, and chronic cardiovascular changes. Hemodialysis AV access causes an acute decrease in systemic vascular resistance and a secondary increase in cardiac output. Although usually clinically insignificant, the increased cardiac output causes heart failure in some patients, particularly those with underlying heart disease or hemodialysis AV access flows (Qa) greater than 2 L/min.

Acute changes — Acute effects of hemodialysis AV access creation include an immediate decrease in systemic vascular resistance and consequent increases in forward stroke volume, heart rate, and cardiac output.

The decrease in total peripheral vascular resistance is due to both changes in the vessels associated with the hemodialysis AV access (called access resistance [AR]) and changes in the systemic vessels (systemic vascular resistance). In response to increases in blood flow and shear stress, the vascular endothelium releases nitric oxide and other endothelium-dependent relaxing factors that dilate the artery, reducing shear stress towards normal [22,23]. One study showed that mean shear stress increased by 475 percent and brachial artery diameter by 15 percent within one day following placement of a radio-cephalic AV fistula [24].

The decrease in systemic vascular resistance causes an acute fall in both central and peripheral blood pressure. In response, there is an increase in sympathetic nervous system activity (which increases contractility and heart rate). It is this combination of decreased cardiac afterload and increased sympathetic activation that causes increases in cardiac output acutely [11,22,25].

The cardiac output increases immediately upon creation of the AV access and continues to increase over time [11,20,26,27]. This increase in cardiac output leads to an increase in venous return to the right side of the heart, leading to right ventricular dilatation in some patients [1]. Conversely, compression of an AV access over days and weeks increases systemic vascular resistance and blood pressure and decreases cardiac output. The increase in pressure leads to baroreflex-mediated reduction in heart rate (Branham's sign).

Subacute and chronic changes — Subacute changes occur within days after creation of the hemodialysis AV access. Within two weeks of AV access creation, blood volume increases, leading to greater venous return and increased right atrial, pulmonary artery, and left ventricular end-diastolic pressures [28]. Both plasma atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) concentrations increase after AV fistula creation, peaking 10 days after AV fistula creation [29].

The cardiac output continues to increase over days and weeks after creating an AV access [11,20,26,27]. In one study of 16 chronic kidney disease (CKD) patients, the cardiac output as assessed by echocardiography increased by 10 percent at 3 days and 14 percent by 14 days after AV fistula placement [29]. In another study of 30 patients, the cardiac output increased by 17 percent two weeks after successful AV fistula surgery [22].

The increase in cardiac output is generally proportional to hemodialysis Qa, although the relationship is complex [11,20]. Hemodialysis Qa is significantly lower for radiocephalic AV fistula compared with brachial-artery-based AV fistula [30]. In one study in which access blood flow was calculated just before the creation of an AV fistula and at days 1, 7, 28, and six months after construction, the most dramatic change occurred at day 1 [31]. By day 28, blood flow had doubled. A further 38.5 percent increase was noted at the last measurement performed after six months.

The increases in cardiac output over days and weeks after creation of an AV access may be one of many factors contributing to the observation that the highest mortality rate for incident hemodialysis patients occurs within the first 120 days after starting hemodialysis [32,33].

Chronic changes occurring over weeks and months in response to the AV access may include the development or worsening of right ventricular dilation and dysfunction, left ventricular hypertrophy (LVH), left atrial dilatation, and pulmonary hypertension [1]. Myocardial remodeling related to volume overload occurs within the first few weeks after AV access creation [29,34,35]. In some cases, left ventricle hypertrophy progresses despite improvements in fluid management and hypertension [36-39]. However, later data suggested that left ventricular chamber size decreased chronically after AV fistula creation, in contrast with the right ventricle, which dilates and may become dysfunctional [1].

Hemodialysis AV access-mediated increases in cardiac output can also increase the risk of pulmonary hypertension [36-38]. This issue is discussed elsewhere. (See "Pulmonary hypertension in patients with end-stage kidney disease".)

CLINICAL MANIFESTATIONS — Symptoms and signs of heart failure may develop after hemodialysis arteriovenous (AV) access creation in patients with or without prior history of heart disease [1,2]. Such patients may show progressive symptoms including dyspnea at rest or with exertion, orthopnea, and fatigue that do not improve with aggressive diuresis or ultrafiltration (if on dialysis) to optimal dry weight or anemia correction. This may occur any time following creation of hemodialysis AV access, from weeks to even years later. It may be more difficult to achieve dry weight on hemodialysis because of intradialytic hemodynamic instability. (See "Heart failure: Clinical manifestations and diagnosis in adults" and "Intradialytic hypotension in an otherwise stable patient", section on 'Decreased cardiac reserve'.)

On physical examination, patients may present with tachycardia, edema, jugular venous distention, a wide pulse-pressure, an enlarged apical impulse, a midsystolic murmur (caused by increased ventricular filling), pulmonary crackles, peripheral edema, and warm extremities as a result of low systemic vascular resistance [40]. However, these dramatic findings of high-output failure may not be evident, and the physical examination may be relatively normal in some patients. (See "Causes and pathophysiology of high-output heart failure".)

MONITORING AND DIAGNOSIS — The evaluation of all patients following hemodialysis arteriovenous (AV) access includes an evaluation for heart failure. All patients who undergo access placement have markedly reduced kidney function and are at risk for heart failure. Patients who are at particular risk to develop heart failure related to the hemodialysis AV access include those with a large, distended AV fistula, especially in the upper-arm position [1,2,9,11,33,40].

Monitoring strategy — The optimal frequency of evaluation is not known. The National Kidney Foundation-Kidney Disease Outcomes Quality Initiative (KDOQI) Clinical Practice Guideline for Vascular Access: 2019 Update recommends regular physical examination or check of the AV access by a knowledgeable and experienced clinician to detect indicators of flow dysfunction [41]. We generally see patients in follow-up at four to six weeks after hemodialysis AV access creation and every four to eight weeks thereafter until the patient starts dialysis.

●We monitor for signs and symptoms of heart failure as a routine part of every visit and determine whether heart failure is present. (See 'Approach to diagnosis' below.)

An echocardiogram should be obtained when any new symptoms or signs suggestive of cardiac dysfunction develop. Echocardiographic findings suggesting the development of heart failure include dilation of the inferior vena cava, new right ventricular dilation or dysfunction, and increasing estimated pulmonary artery pressures.

●We examine the hemodialysis AV access at every visit. The presence of a large, distended AV fistula with very strong pulse augmentation and thrill is suspicious for high blood flow and should prompt a quantitative evaluation, particularly in the presence of heart failure signs and symptoms. (See 'Examination and transient occlusion of AV access' below and "Clinical monitoring and surveillance of hemodialysis arteriovenous grafts to prevent thrombosis", section on 'Intra-access blood flow monitoring' and "Hemodialysis access-induced distal ischemia", section on 'High-flow arteriovenous fistulas'.)

A high-flow AV fistula can be defined as one with a volume flow (Qa) >1.5 L/min. Patients with a Qa >2 L/min are at increased risk for the development of heart failure [11,20]. Blood flow >2 L/min may predict the occurrence of high-output heart failure [11,42]. However, Qa ≤2 L/min does not exclude hemodialysis AV access-induced heart failure. (See "Hemodialysis access-induced distal ischemia", section on 'Quantifying arteriovenous access flow'.)

Approach to diagnosis — For dialysis or predialysis chronic kidney disease (CKD) patients who have hemodialysis AV access and have signs or symptoms of heart failure, we perform a diagnostic evaluation to determine whether heart failure is present, as described separately. It should be noted that hemodialysis and peritoneal dialysis can mask signs and symptoms of heart failure by fluid removal. Evidence suggesting heart failure in these cases may be subtle, and symptoms may not be identified unless specific questions are asked. (See "Heart failure: Clinical manifestations and diagnosis in adults" and "Overview of screening and diagnosis of heart disease in patients on dialysis", section on 'Diagnosis of heart failure'.)

For dialysis or predialysis CKD patients who have hemodialysis AV access and are diagnosed with new-onset or worsening heart failure, we recommend obtaining a comprehensive echocardiogram (ie, with assessment of ejection fraction and cardiac output) and noninvasively measuring access blood flow. Methods for measurement of hemodialysis AV access blood flow are discussed separately. (See "Clinical monitoring and surveillance of hemodialysis arteriovenous grafts to prevent thrombosis", section on 'Intra-access blood flow monitoring'.)

The presence of one or more of the following echocardiographic findings is suggestive of hemodialysis AV access-related heart failure: dilation of the inferior vena cava, right ventricular enlargement or dysfunction, elevation in estimated pulmonary artery pressures, or left ventricular enlargement. Of note, left ventricular ejection fraction can be normal or reduced in patients with hemodialysis AV access-related heart failure.

For patients with hemodialysis AV access with new or worsening heart failure with supportive findings on echocardiography, we suggest invasive evaluation of cardiac hemodynamics by right heart catheterization at rest and with transient AV access occlusion (30 seconds). This allows for definitive assessment of volume status, direct determination of cardiac output and pulmonary artery pressures, and examination of the hemodynamic response, which can provide valuable data when considering management strategies. Transient AV access occlusion should produce a reduction in cardiac output that is often coupled with reduction in central venous pressure. Pulmonary artery and pulmonary capillary wedge pressures may not decrease during transient AV access occlusion, due to the acute increase in cardiac afterload. (See 'Examination and transient occlusion of AV access' below.)

Some studies have suggested assessing the cardio-pulmonary recirculation (CPR) value, which is the ratio of hemodialysis Qa to the cardiac output (CO) in patients with hemodialysis Qa >2 L/min. A Qa:CO ratio >0.3 indicates a significant risk of developing high-output cardiac failure [11,20,42]. However, we do not rely on these indices, since a Qa:CO ratio ≤0.3 or a Qa ≤2 L/min does not exclude access-related heart failure.

We assess cardiac output indexed for body surface area (cardiac index [CI]) but do not use a threshold CI to identify a high-output state. Although high-output heart failure has traditionally been defined as symptoms in the setting of a cardiac output greater than 8 L/min or a CI greater than 4 L/min/m² [2,43], the use of a threshold value for CI is problematic since a CI that one patient may tolerate without problems may be excessive for another having decreased cardiac reserve. (See "Overview of screening and diagnosis of heart disease in patients on dialysis".)

The diagnosis of heart failure due to the hemodialysis AV access is confirmed if improvement is observed with treatment [44]. (See "Heart failure: Clinical manifestations and diagnosis in adults".)

Examination and transient occlusion of AV access — The presence of a large, distended hemodialysis AV fistula or AV graft with very strong pulse augmentation suggests high blood flow and should prompt an evaluation to determine effect of the access on systemic hemodynamics. When the hemodialysis AV access is transiently occluded (30 seconds), the degree of the arterial pulse increase (augmentation) distal to the AV anastomosis is proportional to the Qa. (See "Early evaluation of the newly created hemodialysis arteriovenous fistula", section on 'Perform special maneuvers'.)

Transient maximal occlusion (sphygmomanometer inflated to 50 mmHg above systolic pressure for 30 seconds) of a hemodynamically significant hemodialysis AV access usually decreases heart rate, raises arterial pressure, and lowers venous pressure; this has been termed the Nicoladoni-Branham sign [45]. The Nicoladoni-Branham sign has been shown to be related to arterial baroreceptor activation and increased arterial baroreflex sensitivity [45]. In addition to a decrease in heart rate, there is also an increase in arterial blood pressure and a decrease in cardiac output [45-47]. In a review of 17 patients, increases in systemic vascular resistance and mean arterial blood pressure during pneumatic occlusion of a surgical AV fistula were predictive of a reduction in left ventricular hypertrophy (LVH) after AV fistula ligation [47].

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of hemodialysis arteriovenous (AV) access-related heart failure includes other causes of heart failure (heart failure with preserved ejection fraction [HFpEF] or heart failure with reduced ejection fraction [HFrEF]), including other causes of high-output heart failure. For patients who develop new or worsening heart failure sometime after creation of hemodialysis access, clinical and echocardiographic evaluation should include evaluation for other potential causes of decompensation such as volume overload, left ventricular systolic dysfunction, and valve disease. The evaluation of causes of heart failure is discussed further separately. (See "Determining the etiology and severity of heart failure or cardiomyopathy" and "Heart failure with preserved ejection fraction: Clinical manifestations and diagnosis", section on 'Differential diagnosis' and "Clinical manifestations, diagnosis, and management of high-output heart failure", section on 'Differential diagnosis'.)

PREVENTION — The patient's cardiovascular status should be considered in choosing the dialysis modality, and it is one of the major criteria in selecting the appropriate vascular access type for patients undergoing hemodialysis [30,40,41]. Each patient should be classified using the New York Heart Association functional classification (NYHA classes I to IV) and the American College of Cardiology Foundation/American Heart Association stages of heart failure (ACC/AHA stages A to D) [48,49]. These classifications relate to patient prognosis and the risk associated with an arteriovenous (AV) fistula creation. Patients with end-stage kidney disease (ESKD) with NYHA functional class IV have the highest risk of clinical aggravation and fatal outcome after AV fistula creation [30,40].

Patients with heart failure may benefit more from peritoneal dialysis than in-center hemodialysis [50-54]. Peritoneal dialysis avoids the risks associated with AV access creation and allows better control of volume status because of daily ultrafiltration. However, many variables factor into the decision for peritoneal dialysis, including the patient's ability and willingness to perform the procedure. Although we believe all patients with heart failure should be evaluated for peritoneal dialysis, dialysis modality selection is based upon many factors. (See "Management of heart failure in patients on dialysis", section on 'Dialysis modality'.)

For patients with heart failure who are treated with hemodialysis, the following approach to vascular access selection in patients with ESKD and heart failure is suggested:

●ACC/AHA stage C heart failure with NYHA functional class I or II – Radial-cephalic AV fistula. A brachial artery-based AV fistula should be avoided because it carries the highest risk of worsening the cardiac performance. The best approach is to create a radial-cephalic AV fistula with sufficient blood flow to perform the hemodialysis treatment and, at the same time, with a minimum of hemodynamic impact. In addition, it has been suggested that an end-to-side anastomosis be used when creating a radial-cephalic AV fistula. This has been reported to result in a lower flow compared with a side-to-side anastomosis [21]. (See "Arteriovenous fistula creation for hemodialysis and its complications".)

●ACC/AHA stage C with NYHA functional class III or IV or stage D – Tunneled hemodialysis catheter. For patients with advanced heart failure, insertion of a tunneled central venous hemodialysis access catheter rather than an AV fistula or graft is reasonable given the limited life expectancy for patients with higher stages of heart failure [30]. Patients who use a tunneled catheter are at high risk for infection and should be carefully followed for such. Alternatively, some experts would consider switching these patients from hemodialysis to peritoneal dialysis, although there are no data to support this approach. (See "Central venous catheters for acute and chronic hemodialysis access and their management".)

These measures aim to avoid exposing a patient with heart failure to excessive blood flow. However, as discussed above, cardiac changes associated with the presence of an AV access occur within weeks to months even in the absence of what many would classify as excessive hemodialysis Qa, changes that have been associated with increased patient mortality [55-57] (see 'Subacute and chronic changes' above).

In addition, with the passage of time, patients without heart failure at baseline are at risk for developing heart failure. This raises the question as to whether flow reduction should be considered in patients with significant cardiac changes noted on echocardiography, even in the absence of clinical evidence of heart failure to prevent its development. In a study of 42 asymptomatic patients with cardiac changes, Qa reduction improved cardiac structure and function [58]. Although this was a small study, it suggested that the prevention of high Qa-induced complications is achievable through flow reduction. (See 'Management' below.)

MANAGEMENT — In the patient with hemodialysis arteriovenous (AV) access-related heart failure, management begins with control of volume status with dialysis and diuretics, correction of anemia, treatment of hypertension, and pharmacologic management of heart failure. (See "Overview of screening and diagnosis of heart disease in patients on dialysis".)

If heart failure persists despite attempts to control it with medical therapy, we attempt to reduce the cardiac workload presented by the hemodialysis AV access. We use the following approach:

●Close any unused AV access sites – If the patient has more than one hemodialysis AV access, one should be closed immediately while ensuring preservation of the best AV access to allow adequate kidney replacement therapy, and then reassess the patient's clinical status. Determination of whether the AV fistula is contributing to heart failure is described above. (See 'Approach to diagnosis' above and "Central vein obstruction associated with upper extremity hemodialysis access", section on 'Arteriovenous access occlusion'.)

●Reduce blood flow of the hemodialysis AV access that is used for hemodialysis, if heart failure persists (ie, with no unused fistulas) – To salvage the hemodialysis AV access, we try to reduce its blood flow before considering ligation unless heart failure is severe.

Several different surgical techniques have been used to reduce AV fistula flow. The goal of surgery is to reduce AV access blood flow while maintaining sufficient flow for adequate dialysis. These techniques have included minimally invasive techniques using precision banding [59-63], and open surgical interventions, such as surgical banding or revision of the anastomosis or feeding artery [64-66]. (See "Hemodialysis access-induced distal ischemia", section on 'High-flow arteriovenous fistulas'.)

•In one study of 12 patients with a high-flow AV fistula and clinical signs of high-output heart failure, a precision banding procedure was effective for Qa reduction (see "Hemodialysis access-induced distal ischemia", section on 'Precision banding') [59]. Adequacy of Qa restriction was evaluated intraoperatively using ultrasound flow measurements, adjusting the banding diameter in 0.5 mm increments to achieve the targeted AV fistula flow. Mean Qa was reduced to a mean of 598 mL/min (481 to 876) after banding. The clinical signs of heart failure disappeared, and AV fistulas remained patent in all patients. Two patients had kidney transplant failure and later successfully used the AV fistula. Follow-up postbanding was 1 to 18 months (mean = 12). In another study including 35 patients, AV fistula banding was associated with reductions in left ventricular (LV) size and pulmonary artery pressure as estimated by echocardiography [1]. While there was no reduction in right ventricular size in this study, there was no further progression in remodeling associated with banding.

•In another study, 17 hemodialysis patients with an upper-arm vascular access and heart failure were treated by ligating the brachial artery anastomosis and reconstructing the access using an expanded polytetrafluoroethylene vascular graft in a bypass from the radial artery (ie, revision using distal inflow [RUDI] procedure]) (see "Hemodialysis access-induced distal ischemia", section on 'Revision using distal inflow') [64]. The mean access inflow rate and the mean cardiac output decreased after the inflow reduction procedure, with resolution of symptoms. The median length of follow-up in the series was 16 months. During the follow-up period, thrombosis or stenosis developed in seven patients, three of whom underwent surgical revision. Thirteen of the 17 accesses (77 percent) subjected to the inflow reduction procedure remained patent. Access loss was due to failed fistuloplasty or thrombosis.

•In a six-month prospective, observational study of 25 consecutive hemodialysis patients, there was a decrease in both eccentric and concentric hypertrophy after closure of an AV fistula and placement of a tunneled catheter [67]. The left ventricular ejection fraction also increased in this study. Improvement in cardiac function (and presumably heart failure severity) may be greater in patients with higher cardiac output prior to surgery [68]. Thus the degree to which patients improve may depend more on cardiac output rather than the degree of flow across the hemodialysis AV access site prior to surgery.

●If refractory heart failure persists, close the AV access ─ If the approach defined above is ineffective in managing an AV fistula, we close the AV fistula and place a tunneled catheter or a small AV graft since the resistance is generally higher in AV grafts than fistulas. Given the clear association between heart failure development and the apparent irreversibility of at least some structural features, we would not attempt a lower flow AV fistula, for example, at the radial artery. Peritoneal dialysis may also be an option among some patients. (See "Hemodialysis access-induced distal ischemia", section on 'Arteriovenous access ligation'.)

Evidence supporting the cardiac benefits of AV fistula closure comes from a trial in which 64 patients with a functional kidney transplant were randomly assigned to undergo AV fistula ligation or standard care (ie, no intervention) [69]. All patients underwent a cardiac magnetic resonance imaging prior to and six months following the ligation procedure (or no intervention in the control arm). At six months, LV mass was reduced by 22.1 g (95% CI, 15.0-29.1) in the AV fistula ligation group compared with a small increase of 1.2 g (95% CI, -4.8 to 7.2 g) in the control group. In addition, AV fistula ligation led to reductions in LV volume, RV volume, cardiac output, left atrial volume, and N-terminal pro B-type natriuretic peptide (NT-proBNP) levels. The degree of reduction in LV mass was greater in patients with higher baseline cardiac output (ie, among patients with higher AV fistula flow), suggesting a dose-response effect [70]. None of the patients in this trial experienced allograft failure following closure, but a decline in kidney function following AV fistula closure was reported in another study [71]. While patients in this trial did not have a diagnosis of heart failure at baseline, the reductions in LV mass and volume are clinically meaningful and would be expected to be beneficial in patients with cardiac dysfunction or clinical heart failure.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Heart failure in adults" and "Society guideline links: Hemodialysis vascular access".)

SUMMARY AND RECOMMENDATIONS

●Pathogenesis – Creation of hemodialysis arteriovenous (AV) access (via constructed native AV fistula or prosthetic AV graft) causes an acute decrease in systemic vascular resistance and a secondary increase in cardiac output. Although usually clinically insignificant, the increased cardiac output causes heart failure in some patients, particularly those with underlying heart disease or hemodialysis AV access flows greater than 2 L/min. (See 'Pathogenesis' above.)

●Clinical manifestations – Symptoms and signs of heart failure may develop weeks or years after hemodialysis AV access creation. (See 'Clinical manifestations' above.)

●Monitoring and diagnosis – Monitoring for and diagnosis of hemodialysis AV-access-related heart failure includes identification of at-risk patients, monitoring, identification of symptoms and signs of heart failure, diagnosis of heart failure, and identification of the cause of heart failure.

•The presence of a large, distended hemodialysis AV fistula or AV graft with very strong pulse augmentation is suspicious for high blood flow and should prompt an evaluation for high-output heart failure. When the hemodialysis AV access is transiently occluded, the degree of the arterial pulse increase (augmentation) distal to the AV anastomosis is proportional to the Qa. (See 'Examination and transient occlusion of AV access' above.)

•For patients with hemodialysis AV access with new or worsening heart failure and supportive findings on echocardiography, we suggest invasive evaluation of cardiac hemodynamics by right heart catheterization at rest and with transient AV access occlusion. This allows for definitive assessment of volume status, direct determination of cardiac output and pulmonary artery pressures, and examination of the hemodynamic response to transient AV access occlusion. (See 'Approach to diagnosis' above.)

●Prevention – Regardless of heart failure risk or status, we place a distal radial-cephalic AV fistula rather than a brachial artery AV fistula, if possible. When creating an AV fistula, we generally use an end-to-side anastomosis since this has been reported to result in a lower flow compared with a side-to-side anastomosis. (See 'Prevention' above and "Approach to the adult patient needing vascular access for chronic hemodialysis" and "Arteriovenous fistula creation for hemodialysis and its complications".)

For patients with advanced heart failure (stage C with New York Heart Association [NYHA] functional class III or IV or stage D heart failure) despite optimum therapy), a tunneled hemodialysis catheter is an option given limited life expectancy and risk of access thrombosis due to low blood pressure. Alternatively, some experts would consider switching these patients from hemodialysis to peritoneal dialysis, although there are no data to support this approach. (See 'Prevention' above.)

●Management – For patients with AV-access related heart failure that remains uncontrolled despite medical therapy, we use the following approach:

•Close any unused AV access sites and reassess the patient.

•If heart failure remains refractory, reduce flow of the AV access that is used for hemodialysis and, if refractory heart failure persists, close the hemodialysis AV access. (See 'Management' above.)