High output failure

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Joseph Nasr, M.D.[2]

Overview

In high output cardiac failure, the cardiac output is increased, and the systemic vascular resistance (SVR) is low. Rather than an inadequate supply of blood flow to meet normal metabolic demands as occurs in low output failure, in high output failure there is an excess requirement for oxygen and nutrients and the demand outstrips what the heart can provide.

Conditions to Differentiate High Output Cardiac Failure From

In low cardiac output failure, the cardiac output is reduced, and the systemic vascular resistance (SVR) is high. In low output failure, there is an inadequate supply of blood flow to meet normal metabolic demands.

Differential Diagnosis of High Output Failure

• Anemia
• Arteriovenous fistulae, or arteriovenous malformations
  • Hemodialysis arteriovenous access (arteriovenous fistula or graft) Chronic high-flow hemodialysis access can reduce systemic vascular resistance and increase venous return, resulting in a sustained elevation in cardiac output that may progress to high-output heart failure, particularly in patients with preexisting cardiac disease or very high access flow volumes.
• Beriberi (vitamin B₁/thiamine deficiency
• Paget's disease
• Gram negative septicaemia
• Thyrotoxicosis

Hemodialysis-related high output heart failure

High-output heart failure associated with hemodialysis arteriovenous access results from chronic shunting of blood from the arterial to venous circulation, leading to reduced systemic vascular resistance, increased venous return, and sustained elevation in cardiac output. Over time, this adaptive response may progress to maladaptive ventricular remodeling and symptomatic heart failure.

Risk factors for access-related high-output heart failure include preexisting heart failure, brachial artery–based access, large anastomotic diameter, and high access flow volumes.

Clinical features may include exertional dyspnea, fatigue, peripheral edema, widened pulse pressure, and signs of volume overload. On physical examination, compression of the arteriovenous access may produce transient hypertension and bradycardia (Nicoladoni-Branham sign).

Diagnostic evaluation typically includes echocardiography demonstrating a hyperdynamic circulation with increased cardiac output, elevated cardiac index, and ventricular dilation. Duplex ultrasonography is used to quantify access flow, with values greater than approximately 2000 mL per minute commonly associated with high-output states.

A definitive diagnosis is supported when reduction or elimination of access flow leads to improvement in cardiac function and symptoms.

Management depends on severity of symptoms and ongoing need for dialysis access. Options include flow-reduction procedures such as banding or revision using distal inflow. In patients who no longer require dialysis access, including kidney transplant recipients, access ligation has been shown to improve cardiac structure and function and prevent progressive ventricular remodeling.