Brief review: heart failure as a hemodynamic consequence of high-flow arteriovenous fistulas among end-stage kidney disease patients on hemodialysis.

Hemodialysis remains the predominant kidney replacement therapy modality for patients with end-stage kidney disease. A surgically created arteriovenous fistula (AVF) is the preferred access for hemodialysis and serves as a lifeline for these patients. The creation of a permanent, high-conductance shunt, however, carries hemodynamic consequences in a subset of patients. In certain cases, an enlarging AVF creates a state of "hemodynamic theft," where the shunting of blood through the low-resistance AVF can divert perfusion from the systemic circulation. In these situations, compensatory mechanisms that initially accommodate the increased cardiac workload may eventually fail, transitioning patients into a state of high-output heart failure and secondary pulmonary hypertension. This brief review outlines the pathophysiology of high-output heart failure resulting from AVF enlargement and examines the restoration of cardiovascular stability achieved through surgical banding. By reducing the effective circumference of the fistula or shunt, this intervention may represent an important component of heart failure management and mitigation for this untoward complication of hemodialysis.