An arteriovenous fistula (AVF) is a direct connection between an artery and a vein, bypassing the normal capillary network. This allows high-pressure arterial blood to shunt straight into the low-pressure vein. This abnormal circuit, whether formed naturally or created surgically, significantly impacts the body’s circulatory system. The presence of an AVF is particularly significant in cardiology because this rerouting of blood flow directly alters the workload and function of the heart.
What is an AVF and Why is it Created
An arteriovenous fistula is a passageway connecting an artery and a vein, which are normally separated by the capillary bed. Pathological causes include congenital defects, severe trauma, or the erosion of an arterial aneurysm. However, the most common context for an AVF today is its therapeutic creation by a vascular surgeon.
This surgical procedure establishes reliable vascular access for patients requiring long-term hemodialysis. The high-pressure arterial flow into the vein causes the vein wall to thicken (arterialization), allowing it to withstand the repeated needle punctures necessary for dialysis. This matured AVF provides the high flow rates needed for efficient blood filtration, typically located in the arm or leg.
Hemodynamic Consequences on the Heart
The creation of an AVF introduces a low-resistance pathway into the circulatory system, dramatically altering hemodynamics. Because blood bypasses the high-resistance arterioles and capillaries, the overall systemic vascular resistance (SVR) drops significantly. The heart interprets this decrease in resistance as a sudden need to pump harder to maintain adequate blood pressure and perfusion to the rest of the body.
The heart compensates for this drop in SVR by increasing its cardiac output (CO), resulting in a high-output state. This increase is driven by an elevated heart rate and a greater stroke volume due to increased venous return, or preload, to the heart. In some cases, the AVF can effectively shunt 15 to 20% of the body’s total cardiac output through the new connection.
This chronic demand subjects the heart muscle to relentless strain. The sustained volume overload and excessive workload lead to structural changes, specifically ventricular remodeling. The chambers, particularly the left ventricle, begin to dilate and the muscle walls thicken, a phenomenon called left ventricular hypertrophy.
These structural changes are maladaptive; while they initially help manage the high flow, they eventually impair the heart’s efficiency. This chronic stress can eventually lead to high-output heart failure, where the heart cannot sustain the abnormally high cardiac output required to meet the body’s demands and simultaneously manage the flow through the fistula. This mechanism is particularly concerning for patients who already have underlying cardiovascular disease.
Clinical Recognition of Cardiac Complications
Cardiologists recognize AVF-related cardiac stress through patient symptoms and diagnostic testing. Patients experiencing this high-output state may report symptoms mimicking standard heart failure, such as shortness of breath (dyspnea), general fatigue, and swelling (edema) in the extremities. Physical examination may reveal an abnormally fast heart rate (tachycardia) and a wide pulse pressure caused by the rapid runoff of blood into the low-resistance venous system.
Clinicians often hear a continuous whooshing sound, known as a bruit, directly over the fistula site. Diagnostic imaging is essential to quantify the cardiac impact. Echocardiography provides a non-invasive assessment of the heart’s structure, revealing signs like left ventricular dilation and hypertrophy indicative of chronic volume overload.
To pinpoint the AVF as the cause, specialized non-invasive ultrasound is used to measure the fistula’s flow rate (Qa). A flow rate exceeding 2,000 milliliters per minute is often considered a high-flow AVF that carries a greater risk of high-output heart failure. Blood tests may also show elevated levels of natriuretic peptides, such as NT-proBNP, which are biomarkers released in response to increased cardiac wall stress and volume expansion.
Treatment Strategies for AVF-Induced Heart Strain
Managing AVF-induced heart strain requires a collaborative approach among cardiology, nephrology, and vascular surgery. Initial treatment involves standard medical management for heart failure, using medications like diuretics to control fluid overload and beta-blockers or ACE inhibitors to reduce the heart’s workload. However, these medications only manage the symptoms and do not address the underlying flow problem.
The definitive strategy focuses on reducing blood flow through the fistula to lessen the cardiac burden. One common intervention is flow reduction, often accomplished through a surgical technique called banding. This procedure physically narrows the fistula to decrease the volume of blood shunted. The goal is a flow rate low enough to relieve heart strain but high enough to maintain the fistula’s usability for dialysis.
Complete closure, or ligation, of the AVF is reserved for patients with severe heart failure refractory to other treatments. This is a significant decision, as it sacrifices vascular access, often necessitating a new, more distal fistula or the use of a central venous catheter for dialysis. Intervention decisions must carefully balance the need for functioning dialysis access against protecting the heart from irreversible damage.