What is high-output heart failure?

High-Output Heart Failure: Definition and Clinical Entity

High-output heart failure is a distinct clinical syndrome where patients present with typical heart failure symptoms and signs (dyspnea, edema, elevated jugular venous pressure) despite an elevated cardiac output (>8 L/min or cardiac index >4 L/min/m²), caused by underlying conditions that reduce systemic vascular resistance or create arteriovenous shunting rather than primary myocardial dysfunction. 1, 2, 3, 4

Pathophysiological Mechanism

The fundamental abnormality in high-output heart failure is not intrinsic myocardial disease but rather circulatory derangements that eventually overwhelm the heart 2, 5:

• Primary problem: Reduced systemic vascular resistance due to either arteriovenous shunting or peripheral vasodilation 5
• Compensatory response: The fall in systemic arterial blood pressure triggers neurohormonal activation (renin-angiotensin-aldosterone system, sympathetic nervous system) leading to volume expansion and increased cardiac work 5
• Cardiac remodeling: Progressive elevation of cardiac output eventually leads to eccentric left ventricular remodeling, four-chamber cardiac enlargement, elevated filling pressures, and overt clinical heart failure 3, 4

Common Etiologies

The most frequent causes include 1, 2, 4:

• Liver disease/cirrhosis (23% of cases) 2, 4
• Arteriovenous shunts/fistulas (23% of cases), including dialysis access fistulas 2, 6, 4
• Severe chronic anemia 1, 2
• Thyrotoxicosis/hyperthyroidism (can increase cardiac output up to 300% from baseline) 1, 2
• Obesity (31% of cases in modern series) 4
• Septicemia/sepsis 1, 2
• Paget's disease of bone 1, 2
• Beriberi (thiamine deficiency) 2
• Myeloproliferative disorders (8% of cases) 4

Clinical Presentation

Patients with high-output heart failure are clinically indistinguishable from other forms of heart failure 2:

• Typical symptoms: breathlessness, fatigue, ankle swelling, orthopnea 1, 2
• Physical examination findings: tachycardia, elevated jugular venous pressure, warm peripheries (unlike low-output failure), pulmonary congestion, peripheral edema 1
• Key distinguishing feature: Warm extremities with bounding pulses, contrasting with the cool extremities seen in low-output cardiogenic shock 1

Hemodynamic Characteristics

The European Society of Cardiology defines the hemodynamic profile as 1:

• Elevated cardiac output/cardiac index 1, 4
• Reduced systemic vascular resistance (lowest SVR associated with poorest outcomes) 4
• Elevated pulmonary capillary wedge pressure 1, 4
• Variable blood pressure (can be low due to vasodilation despite high cardiac output) 1
• Preserved or normal ejection fraction initially, though eccentric remodeling develops over time 4

Diagnostic Clues

Echocardiographic findings suggesting high-output heart failure include 1, 2, 4:

• Four-chamber cardiac enlargement 1, 2
• Increased left ventricular outflow tract velocity-time integral 1
• Eccentric left ventricular remodeling 4
• Preserved ejection fraction 4

Critical diagnostic approach: Actively search for underlying reversible causes through targeted testing based on clinical suspicion, including thyroid function tests, complete blood count for anemia, liver function tests, and vascular imaging for arteriovenous malformations 1, 2, 4

Management Principles

Primary Treatment Strategy

The cornerstone of management is treating the reversible underlying etiology 2, 5:

• Correct anemia (transfusion, iron supplementation, erythropoietin) 2, 5
• Treat thyrotoxicosis 2, 5
• Close arteriovenous fistulas or malformations (surgical ligation or endovascular embolization) 2, 6, 7
• Manage liver disease 2, 5
• Treat sepsis 2

Symptomatic Management

For fluid overload symptoms 2, 5:

• Dietary sodium and water restriction 2, 5
• Judicious use of diuretics 2, 5

Critical Management Pitfalls

Conventional heart failure therapies can be harmful in high-output heart failure 5:

• Avoid or use cautiously: ACE inhibitors, angiotensin receptor blockers, and vasodilating beta-blockers, as these further reduce systemic vascular resistance and can cause clinical deterioration 5
• Do not use: Beta-adrenoceptor positive inotropes are not recommended 5
• Vasodilators are contraindicated in this setting, unlike typical heart failure management 5

Prognosis

• Mortality is significantly increased compared to controls (hazard ratio 3.4; 95% CI 1.6-7.6) 4
• Poorest outcomes occur in patients with the lowest systemic vascular resistance 4
• Prognosis improves substantially when the underlying cause is corrected (e.g., cardiac output decreased from 19.5 to 9.8 L/min after arteriovenous malformation embolization with corresponding clinical improvement) 7