What is high output heart failure?

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What is High-Output Heart Failure?

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 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 disease. 1, 2

Key Distinguishing Features

High-output heart failure fundamentally differs from typical heart failure because the primary abnormality is not intrinsic heart disease but rather conditions that mimic heart failure through circulatory mechanisms 1:

  • The heart itself may be structurally normal or show eccentric remodeling rather than primary cardiomyopathy 2
  • Cardiac output is elevated (>8 L/min) rather than reduced 2, 3
  • Systemic vascular resistance is markedly decreased 4, 2
  • These conditions are often treatable and should be excluded when diagnosing heart failure 1

Underlying Pathophysiology

The mechanism involves a progressive cascade 4, 2, 5:

  • Primary problem: Reduced systemic vascular resistance from either arteriovenous shunting or peripheral vasodilation 4
  • Compensatory response: Fall in systemic arterial blood pressure triggers neurohormonal activation (renin-angiotensin-aldosterone system, neprilysin, sodium-glucose-2 transporter) 4, 5
  • Consequence: Salt and water retention, interstitial fibrosis, ventricular remodeling, and eventually overt clinical heart failure despite elevated cardiac output 5
  • The elevated cardiac output results from both lower arterial afterload (decreased systemic vascular resistance) and higher metabolic rate 2

Common Etiologies

The most frequent causes in modern practice are 1, 2:

  • Obesity (31% of cases) 2
  • Liver disease/cirrhosis (23%) 1, 2
  • Arteriovenous shunts/fistulas (23%) 1, 2
  • Chronic lung disease (16%) 2
  • Anemia 1, 4
  • Thyrotoxicosis 1, 4
  • Septicemia 1
  • Myeloproliferative disorders (8%) 2
  • Paget's disease 1
  • Beri-beri (thiamine deficiency) 1

Clinical Presentation

Patients present with typical heart failure symptoms and signs that are indistinguishable from other forms of heart failure 1, 2:

  • Breathlessness at rest or on exercise, fatigue, tiredness, ankle swelling 1
  • Tachycardia, tachypnea, pulmonary rales, pleural effusion, raised jugular venous pressure, peripheral edema, hepatomegaly 1
  • Elevated natriuretic peptides 2
  • Preserved or normal ejection fraction in many cases 2, 3

Two Distinct Phenotypes

Modern understanding recognizes two phenotypes regardless of etiology 5:

  1. Dilated phenotype: Enlarged cardiac chambers with eccentric left ventricular remodeling 2, 5
  2. Non-dilated phenotype: Normal-sized heart chambers despite elevated output 5

The phenotype depends on disease evolution rather than specific etiology 5.

Diagnostic Clues

Echocardiographic findings suggesting high-output heart failure include 1:

  • Four-chamber cardiac enlargement 1
  • Increased left ventricular outflow tract velocity-time integral (VTI) 1
  • Preserved ejection fraction despite heart failure symptoms 2, 3

Hemodynamic assessment reveals 2:

  • Cardiac output >8 L/min or cardiac index >4 L/min/m² 2, 3
  • Elevated filling pressures 2
  • Pulmonary hypertension 2
  • Markedly reduced systemic vascular resistance 2

Critical Management Implications

Treatment differs fundamentally from conventional heart failure 4, 3:

  • Conventional vasodilator therapies (ACE inhibitors, ARBs, certain beta-blockers with vasodilatory properties) are contraindicated as they further reduce systemic vascular resistance and cause clinical deterioration 4, 3
  • Primary treatment is addressing the underlying cause (correcting anemia, treating thyrotoxicosis, closing arteriovenous fistulas, managing liver disease) 1, 4
  • When no remediable cause exists, therapeutic options are limited to dietary salt and water restriction with judicious diuretics 4
  • Vasodilators and beta-adrenoceptor positive inotropes are not recommended 4

Clinical Significance and Prognosis

High-output heart failure carries substantial mortality 2:

  • Mortality is increased 3.4-fold compared to controls (95% CI: 1.6-7.6) 2
  • Hemodynamics and outcomes are poorest among patients with the lowest systemic vascular resistance 2
  • Given the increasing prevalence of obesity, liver disease, and arteriovenous shunts in Western countries, high-output heart failure must be considered in the differential diagnosis of patients presenting with dyspnea, congestion, and normal ejection fraction 2

Common Pitfall

The most critical error is failing to recognize high-output heart failure and inappropriately applying guideline-directed medical therapy for heart failure with reduced or preserved ejection fraction 3. This leads to worsening hypotension and clinical deterioration due to further reduction in systemic vascular resistance 4, 3. Always investigate for reversible causes when encountering heart failure with preserved ejection fraction, particularly in the presence of conditions known to cause high-output states 1.

References

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

Research

High-Output Heart Failure: A 15-Year Experience.

Journal of the American College of Cardiology, 2016

Research

High output heart failure.

QJM : monthly journal of the Association of Physicians, 2009

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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