Do patients with an Arteriovenous (AV) fistula develop volume overload following a supraclavicular block?

Supraclavicular Block and Volume Overload in AV Fistula Patients

Patients with arteriovenous fistulas do not develop volume overload as a direct consequence of supraclavicular block; however, the underlying AV fistula itself can cause high-output heart failure and volume overload, which may be unmasked or worsened during the perioperative period.

Mechanism of Volume Overload in AV Fistula Patients

The concern about volume overload in AV fistula patients relates to the fistula itself, not the regional anesthetic technique:

• High-output heart failure (HOHF) occurs when AV fistula flow exceeds 5 L/min, defined by cardiac output >8 L/min, resting cardiac index >2.5-4.0 L/min/m², and low systemic vascular resistance 1
• The increased cardiac output from the extracardiac shunt may result in overt heart failure in patients with underlying heart disease 1
• Volume overload manifests as dyspnea, peripheral edema, and signs of congestive heart failure, particularly in patients with pre-existing cardiac disease 1

Effects of Supraclavicular Block on AV Fistula Hemodynamics

Supraclavicular brachial plexus block actually produces vasodilation, not volume overload:

• Mean brachial artery diameter increases by 0.09 mm and cephalic vein diameter increases by 0.5 mm following supraclavicular block 2
• Vein diameter increases are most pronounced in the lower cephalic (34%), upper cephalic (24.2%), and basilic veins (31.3%) 3
• This vasodilation improves operative conditions and may enhance native fistula placement rates from 89% to 93% 3
• The block achieves good immediate patency (93.45%) and long-term patency at 3 months 2

Actual Complications of Supraclavicular Block in This Population

The real risks of supraclavicular block in AV fistula patients are respiratory and vascular, not volume overload:

• Phrenic nerve palsy causing ipsilateral hemidiaphragmatic paralysis can lead to acute hypercapnic respiratory distress with loss of consciousness 4
• Arterial dissection is a rare but catastrophic complication, particularly in patients with hypertension, diabetes, and chronic renal disease 5
• Smoking, hypertension, diabetes mellitus, and chronic calcineurin inhibitor intake predispose patients to iatrogenic arterial dissection 5

Critical Clinical Distinction

The key pitfall is confusing pre-existing volume overload from the AV fistula with a complication of the block itself:

• If a patient presents with signs of volume overload (dyspnea, peripheral edema, elevated jugular venous pressure), this represents high-output heart failure from excessive fistula flow, not a block complication 1
• Central venous stenosis causing venous hypertension can also produce arm swelling and edema, which should be evaluated with fistulography if persistent beyond 2 weeks 6
• Physiological swelling within the first week after AVF placement is normal and resolves with arm elevation and rest 6

Monitoring Recommendations

For patients with AV fistulas undergoing supraclavicular block:

• Assess fistula flow preoperatively using ultrasound Doppler; flows >5 L/min indicate risk for high-output heart failure 1
• Monitor for respiratory complications including phrenic nerve palsy, which can be detected by M-mode ultrasonography of the diaphragm 4
• Evaluate cardiac status in patients with underlying heart disease, as they are at highest risk for decompensation from high-output states 1
• Monthly flow measurements and physical examination are recommended for patients at risk for HOHF 1

Management of True Volume Overload

If volume overload from the AV fistula is present or develops:

• Treatment involves flow reduction procedures, AVF banding, or ligation rather than modification of anesthetic technique 1
• Cardiac catheterization is often required for definitive diagnosis of HOHF 1
• Early recognition is critical as many cases are reversible with appropriate intervention 1