What is high output cardiac failure?

High-Output Heart Failure: Definition and Pathophysiology

High-output heart failure is a clinical syndrome where patients present with typical heart failure symptoms and signs (dyspnea, fatigue, edema, elevated jugular venous pressure) despite having an elevated cardiac output, caused by conditions that reduce systemic vascular resistance or create arteriovenous shunting rather than primary myocardial dysfunction. 1

Core Pathophysiological Mechanism

The fundamental abnormality is not intrinsic cardiac disease but rather circulatory derangements that mimic heart failure 1:

• Reduced systemic vascular resistance from peripheral vasodilation or arteriovenous shunting threatens arterial blood pressure 2, 3
• This triggers neurohormonal activation (renin-angiotensin-aldosterone system, neprilysin, sodium-glucose-2 transporter) 4
• Resulting in renal sodium and water retention, interstitial fibrosis, and ventricular remodeling 4
• The heart itself is typically normal and capable of generating very high cardiac output (>8 L/min) 2, 4
• Increased erythropoietin release can further expand circulating blood volume by up to 25% 5

Common Etiologies

The most frequent causes include 1, 5:

• Severe chronic anemia
• Thyrotoxicosis/hyperthyroidism (can increase cardiac output up to 300% from baseline) 5
• Arteriovenous fistulas or malformations (including hereditary hemorrhagic telangiectasia) 6, 7
• Liver disease/cirrhosis
• Sepsis/septicemia
• Paget's disease of bone
• Thiamine deficiency (Beri-beri)

Clinical Presentation

Patients are clinically indistinguishable from other forms of heart failure 1:

• Dyspnea, increased fatigability, tachypnea 2
• Tachycardia, elevated jugular venous pressure 1
• Peripheral edema, pulmonary rales 2
• The key difference is the elevated cardiac output rather than the typical low output state

Two Distinct Phenotypes

Recent evidence identifies two phenotypes regardless of etiology 4:

1. Dilated phenotype: Enlarged cardiac chambers with four-chamber cardiac enlargement 1, 4
2. Non-dilated phenotype: Normal heart chamber size despite high output 4

Diagnostic Approach

Echocardiographic clues suggesting high-output heart failure 1:

• Four-chamber cardiac enlargement (in dilated phenotype)
• Increased left ventricular outflow tract velocity-time integral
• Cardiac output >8 L/min (can reach 19.5 L/min in severe cases) 7, 4

Look for underlying causes through targeted testing based on clinical suspicion 5:

• Thyroid function tests for hyperthyroidism
• Complete blood count for anemia
• Liver function tests for cirrhosis
• CT angiography or conventional angiography for arteriovenous malformations 7

Management Principles

Primary Treatment: Address the Underlying Cause

The cornerstone of management is treating the reversible etiology 1:

• Correct anemia with transfusion or iron/B12/folate supplementation
• Treat thyrotoxicosis with antithyroid medications, radioactive iodine, or surgery 5
• Close arteriovenous fistulas surgically or via transcatheter embolization 6, 7
• Manage liver disease appropriately
• Treat sepsis with antibiotics and source control 5

Symptomatic Management

For fluid overload 3:

• Dietary sodium and water restriction
• Judicious use of diuretics (avoid excessive preload reduction)

Critical Pitfall: Avoid Standard Heart Failure Therapies

Conventional heart failure medications can worsen high-output heart failure 2, 3:

• Do NOT use vasodilators (ACE inhibitors, ARBs, nitrates) as they further reduce systemic vascular resistance and can cause hemodynamic deterioration 3
• Avoid beta-blockers with vasodilatory properties 3
• Beta-adrenoceptor positive inotropes are not recommended 3

These agents are contraindicated because the underlying problem is already reduced afterload, not inadequate cardiac contractility 2.

Prognosis

Many etiologies are potentially curable with proper identification and treatment 4, 3. Prompt recognition and addressing the underlying cause leads to significant improvement in cardiac output and clinical status 7. Without a remediable cause, therapeutic options remain very limited 3.