High Output Cardiac Failure
High output cardiac failure is a clinical syndrome where patients develop typical heart failure symptoms and signs despite an elevated cardiac output (cardiac index >4 L/min/m²), caused by pathologically reduced systemic vascular resistance from either arteriovenous shunting or peripheral vasodilation, rather than primary myocardial disease. 1, 2
Pathophysiology
The fundamental abnormality in high output cardiac failure is not intrinsic heart disease but rather excessive reduction in systemic vascular resistance that triggers a cascade of compensatory mechanisms 2, 3:
- Reduced systemic vascular resistance occurs through two primary mechanisms: arteriovenous shunting (bypassing capillary beds) or direct peripheral vasodilation 2, 4
- The fall in systemic arterial blood pressure activates neurohormonal systems (renin-angiotensin-aldosterone, sympathetic nervous system) leading to sodium and water retention 2, 4
- This volume expansion combined with the low afterload state forces the heart to maintain abnormally high cardiac output (typically >8 L/min) to maintain adequate perfusion pressure 4
- Despite elevated cardiac output, patients develop classic heart failure symptoms because the compensatory mechanisms eventually fail, leading to congestion and organ dysfunction 2, 3
Common Etiologies
The most frequent causes in modern practice are obesity (31-36%), liver disease/cirrhosis (17-23%), arteriovenous shunts (23%), and lung disease (16-32%) 1, 5, 3:
- Anemia (particularly chronic severe anemia) 1, 5
- Thyrotoxicosis 1
- Septicemia 1
- Arteriovenous fistulas (surgical, traumatic, or congenital) 1, 3
- Paget's disease of bone 1
- Beriberi (thiamine deficiency) 1
- Myeloproliferative disorders (8%) 3, 6
Clinical Phenotypes
Two distinct phenotypes exist regardless of etiology 4:
- Dilated phenotype: Enlarged cardiac chambers with eccentric left ventricular remodeling, similar to traditional heart failure 3, 4
- Non-dilated phenotype: Normal-sized heart chambers despite elevated output, increasingly recognized in liver disease, obesity, and arteriovenous fistulas 4
Hemodynamic Characteristics
Patients demonstrate specific hemodynamic patterns that distinguish this from low-output heart failure 3:
- Cardiac index >4 L/min/m² (diagnostic threshold) with some patients reaching >8 L/min 5, 3, 4
- Markedly reduced systemic vascular resistance (the primary driver) 2, 3
- Elevated filling pressures despite preserved or normal ejection fraction 3
- Pulmonary hypertension is commonly present 3
- Increased metabolic rate contributes to the elevated cardiac output alongside reduced afterload 3
Critical Management Principles
This condition requires fundamentally different treatment than typical heart failure because standard heart failure therapies can be harmful 1, 2:
What NOT to Do:
- Avoid ACE inhibitors, ARBs, and vasodilating beta-blockers as these further reduce systemic vascular resistance and worsen hypotension 2
- Avoid positive inotropes (dobutamine, milrinone) which are contraindicated as they increase cardiac work without addressing the underlying problem 2
- Do not treat as typical heart failure with preserved ejection fraction using guideline-directed medical therapy 1
Appropriate Management:
- Identify and treat the underlying cause - this is potentially curative in many cases (correct anemia, treat thyrotoxicosis, close arteriovenous fistulas, manage liver disease) 1, 2
- Dietary sodium and water restriction combined with judicious diuretic use for symptomatic congestion 2
- These conditions should be excluded when diagnosing primary heart failure and are better labeled as "heart failure secondary to circulatory high output conditions" 1
Prognosis
High output cardiac failure carries significant mortality risk 5, 3:
- Mortality of 25% at median 31.5 months follow-up in patients with cardiac index >4 L/min/m² 5
- Hazard ratio of 3.4 (95% CI: 1.6-7.6) compared to controls 3
- Outcomes are poorest in patients with the lowest systemic vascular resistance 3
- High rates of hospitalization are common 5
Clinical Pitfall
The major diagnostic error is misclassifying these patients as heart failure with preserved ejection fraction and initiating standard heart failure therapies that worsen their hemodynamic state. Always measure cardiac output (via right heart catheterization or non-invasive methods) and systematically evaluate for reversible high-output causes when encountering heart failure symptoms with preserved ejection fraction 1, 2, 3.