High Output Heart Failure Due to Arteriovenous Access in Hemodialysis Patients: Overflowing and Overlooked

Fluid overload is a common problem in patients on maintenance hemodialysis and is frequently associated with increased hospitalizations and cardiovascular mortality. In some studies, the prevalence of fluid overload in ESRD is reported to be 40-70% (1). Excessive salt and fluid intake, nonadherence to dialysis treatments, and underlying comorbidities such as heart failure and cardiovascular disease are the most common reasons for persistent fluid overload in this patient population. About 10% of all hospitalizations in ESRD patients are due to fluid overload, and  1 in 3 patients require rehospitalization within 30 days of discharge, increasing morbidity and financially burdening the healthcare system (2).

Although traditional risk factors such as diabetes, hypertension, hyperlipidemia, and advanced age increase the risk of heart failure and fluid overload in patients with ESRD, certain specific risk factors in the ESRD population, like anemia and hypoalbuminemia also contribute to heart failure and fluid overload. Another specific factor, although commonly known but often overlooked, is the arteriovenous fistula (AVF) or an arteriovenous graft (AVG) in hemodialysis patients. 

The adoption of AVF and AVG as the access of choice has revolutionized the treatment of hemodialysis patients. These accesses provide a lower pressure and a lower vascular resistance circuit, thereby allowing increased blood flow into the access, improving dialysis efficiency, and reducing the risk of infection. However, creating this low-pressure, low vascular resistance circuit in parallel to the high-pressure, high vascular resistance peripheral arterial circuit may cause significant shunting of the blood from the high-pressure arterial circuit to the low-pressure circuit of AVF/AVG, leading to a decrease in the overall systemic vascular resistance and increase in venous return and stroke volume (Figure 1). This can lead to an increase in cardiac output by as much as 10-20%, predisposing to high-output heart failure (HOHF) over time (3). Several studies suggest that AVF/AVG creation may exacerbate underlying heart failure in CKD/ESRD patients or may be an independent risk factor for new onset heart failure in this population(4). Surprisingly, the prevalence of AVF-induced HOHF is not known, as it is often unrecognized or underreported.

Figure 1. Hemodynamic changes associated with high flow AV access that precipitate high output heart failure (HOHF)

The diagnosis of HOHF due to AVF/AVG requires a very high index of suspicion as clinical symptoms or signs of heart failure cannot reliably differentiate HOHF from low or normal cardiac output heart failure. Transient occlusion of the AVF for 15-30 secs to measure changes in heart rate and BP (Barnham sign) in a clinical setting is not always feasible and is often met with skepticism from the patients and dialysis staff. 2D echocardiogram findings that may offer clues of HOHF include dilated IVC, RV, LV dilatation, and elevated right ventricular systolic pressures.  Ejection fraction may be variable in these patients. Definitive diagnosis requires right heart catheterization to measure cardiac index, left ventricular end-diastolic pressure, pulmonary arterial pressure, and central venous pressure. A cardiac index (CI)  of >3.9L/min/m2 or a cardiac output of > 8L/min is diagnostic of HOHF (normal CI 2.5-3.9L/min/m2, normal CO < 8L/min) (5).

Figure 2. Relationship between access flow and cardiac output in hemodialysis patients with AVF.

Source: (Kroon et al., Med Biol Eng Comput (2012) 50:1289–1298 and Basile et al., Nephrol. Dial. Transplant, Jan. 2008)

In such patients with HOHF, a Doppler assessment of the vascular blood flow (Qa) through hemodialysis access may suggest the underlying etiology. Qa over 2L/min in HOHF is often suggestive of HOHF due to AVF and is often more common in proximally located AVF ( avg Qa <1.5L/min) as compared to distal AVF (average Qa < 0.9L/min). However, if a high index of suspicion exists despite Qa <2L/min, in such cases, AVF-induced HOHF should still be considered if the vascular access flow exceeds >30% of the total cardiac output, with blood flow (Qa)/cardiac output (CO) ratio ( cardiopulmonary recirculation rate) of greater than 0.30 triggering further cardiac testing, including right heart catheterization (6). 

Surgical banding of the AV fistula by incrementally reducing the fistula diameter to achieve the desired access blood flow is often curative of HOHF in these patients and, in refractory cases, may need ligation of AVF/AVG. However, prevention and monitoring is key. Regular monitoring of vascular access flow (Qa) may help prompt an early cardiac evaluation. It is better to avoid proximal AVF placement in patients with an underlying history of heart failure, and it may be best to avoid AVF/AVG placement altogether in patients with advanced heart failure with a limited life span, provided the benefits of HD catheters exceed the risk of infection, and this requires a multidisciplinary approach. Contrary to popular belief, peritoneal dialysis may be a preferred option in managing fluid overload and is often better tolerated in these patients (7). 

Therefore, it is essential not to overlook heart failure caused by AVF/AVG in dialysis patients who often present with unexplained fluid overload. High vascular access flow (Qa > 2L/min or Qa/CO >0.3) should trigger further cardiac workup, including right heart catheterization. A close collaboration between nephrologists, cardiologists, and vascular surgeons may help offer the best options to ESRD patients at high risk of this condition.

References:

1. C. Zoccali et al., “Chronic fluid overload and mortality in ESRD,” J. Am. Soc. Nephrol., vol. 28, no. 8, pp. 2491–2497, Aug. 2017.

2. T. Lopez and D. Banerjee, “Management of fluid overload in hemodialysis patients,” Kidney Int., vol. 100, no. 6, pp. 1170–1173, Dec. 2021.

3. R. S. Chang, J.-R. Hu, J. A. Beckman, R. C. Forbes, S. H. Shawar, and B. P. Concepcion, “High output heart failure associated with arteriovenous fistula in the setting of kidney transplantation,” Kidney Int. Rep., vol. 6, no. 2, pp. 544–551, Feb. 2021.

4. H. Wasse and M. S. Singapuri, “High-output heart failure: how to define it, when to treat it, and how to treat it,” Semin. Nephrol., vol. 32, no. 6, pp. 551–557, Nov. 2012.

5. C. Basile, C. Lomonte, L. Vernaglione, F. Casucci, M. Antonelli, and N. Losurdo, “The relationship between the flow of arteriovenous fistula and cardiac output in hemodialysis patients,” Nephrol. Dial. Transplant, vol. 23, no. 1, pp. 282–287, Jan. 2008.

6. E. Wijnen et al., “The relation between vascular access flow and different types of vascular access with systemic hemodynamics in hemodialysis patients,” Artif. Organs, vol. 29, no. 12, pp. 960–964, Dec. 2005.

7. C. Y. Chionh, A. Clementi, C. B. Poh, F. O. Finkelstein, and D. N. Cruz, “The use of peritoneal dialysis in heart failure: A systematic review,” Perit. Dial. Int., vol. 40, no. 6, pp. 527–539, Nov. 2020.