How can a femoral arteriovenous (AV) fistula cause an increased cardiac index measured by a Swan‑Ganz catheter?

How a Femoral AV Fistula Causes Increased Cardiac Index on Swan-Ganz Catheter

A femoral arteriovenous fistula creates a low-resistance shunt that diverts blood directly from the arterial to venous system, bypassing the capillary bed, which forces the heart to increase cardiac output to maintain systemic perfusion—this elevated cardiac output is measured as an increased cardiac index by the Swan-Ganz catheter.

Pathophysiologic Mechanism

Creation of a Low-Resistance Shunt

• An AV fistula establishes an abnormal connection between the arterial and venous systems that completely bypasses the normal anatomic capillary beds 1, 2.
• This creates a pathway of significantly lower resistance compared to the normal systemic vascular resistance, effectively "stealing" blood flow from the systemic circulation 3.
• The femoral location is particularly prone to iatrogenic AVF formation because the profunda femoris vein crosses laterally behind the proximal superficial femoral artery, making simultaneous puncture of both vessels possible during catheterization procedures 2.

Hemodynamic Consequences

• The low-resistance shunt causes immediate recirculation of oxygenated arterial blood back into the venous system without delivering oxygen to tissues 1, 4.
• To compensate for this "wasted" cardiac output and maintain adequate tissue perfusion, the heart must increase its total output through increased stroke volume and/or heart rate 4.
• This compensatory increase in cardiac output is what the Swan-Ganz catheter measures as an elevated cardiac index 4.

Volume Overload Effects

• The continuous shunting of blood increases venous return to the right heart, creating a volume overload state 4.
• This increased preload further stimulates the heart to pump more vigorously through the Frank-Starling mechanism 4.
• In significant fistulas, this can progress to high-output cardiac failure with congestive symptoms, though this typically requires large, persistent fistulas 4.

Clinical Recognition

Physical Examination Findings

• A continuous bruit and palpable thrill at the femoral access site are pathognomonic for AVF 5, 6.
• Active pulsatile bleeding or persistent oozing around the catheter site may indicate AVF formation 6.
• The presence of these findings should prompt immediate duplex ultrasonography for confirmation 3.

Incidence and Risk Factors

• Iatrogenic femoral AVF occurs in approximately 0.86% (nearly 1%) of cardiac catheterization procedures 3.
• Independent risk factors include: high heparin dosage (OR 2.88), coumadin therapy (OR 2.34), left groin puncture (OR 2.21), arterial hypertension (OR 1.86), and female gender (OR 1.84) 3.
• Most AVFs (approximately 38%) close spontaneously within 12 months, though larger fistulas may persist and cause symptoms 3.

Important Clinical Pitfalls

Misdiagnosis Risk

• Symptoms of high-output cardiac failure from a large AVF can be mistaken for other conditions, including chronic fatigue syndrome, as the hemodynamic effects may develop gradually over time 4.
• The fistula can present many years after the initial catheterization procedure, making the connection to the original intervention less obvious 4.

Swan-Ganz Interpretation Error

• An elevated cardiac index in the presence of a femoral AVF does not represent true effective systemic perfusion—much of the measured cardiac output is being "wasted" through the shunt 4.
• Clinicians must recognize that tissue oxygen delivery may be inadequate despite a seemingly normal or elevated cardiac index 4.
• The cardiac index measurement reflects total cardiac output, not effective tissue perfusion, which is a critical distinction in this scenario 4.

Management Considerations

• While most small AVFs close spontaneously and cardiac volume overload is unlikely with small fistulas, conservative management for at least one year is reasonable for asymptomatic patients 3.
• However, symptomatic fistulas causing hemodynamic compromise require intervention—either endovascular coil embolization or open surgical repair 1, 6, 4.
• Intensified anticoagulation may extend AVF persistence and should be minimized when possible 3.