Episode 221: High-Output Heart Failure

We discuss the diagnosis and treatment of one of EM's paradoxes: High-Output Heart Failure.

Hosts:

Nicolas Gonzalez, MD

Brian Gilberti, MD

https://media.blubrry.com/coreem/content.blubrry.com/coreem/HOHF.mp3

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Tags: Cardiology

Show Notes

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1. Core Definition & Hemodynamic Profile

Clinical Paradox: Congestive symptoms (pulmonary edema, JVD, peripheral edema) in the setting of a hyperdynamic, supranormal cardiac function.

Hemodynamic Criteria:

Cardiac Index (CI): >4.0 L/min/m2.

Cardiac Output (CO): >8 L/min.

Systemic Vascular Resistance (SVR): Pathologically low (vasodilated or shunted state).

The “Warm” Phenotype: Unlike standard HFrEF/HFpEF (often “Cold and Wet”), HOHF presents as “Warm and Wet” due to low SVR and bounding pulses.

2. Pathophysiology: The Hemodynamic Paradox

Primary Insult: Decreased SVR (either via peripheral vasodilation or arteriovenous shunting).

Effective Arterial Blood Volume: Paradoxically low despite high total CO.

Neurohormonal Cascade:

Activation of Renin-Angiotensin-Aldosterone System (RAAS).

Increased Sympathetic Nervous System tone.

Increased Antidiuretic Hormone (ADH) secretion.

Resultant State: Avid renal salt and water retention leading to massive plasma volume expansion.

Cardiac Response: Chronic volume overload → eccentric remodeling → chamber dilation → eventual secondary myocardial failure/dilated cardiomyopathy.

3. Differential Diagnosis: Etiological “Buckets”

Category A: Increased Metabolic Demand (Systemic)

Hyperthyroidism/Thyrotoxicosis:

Direct T3 effects: increased chronotropy/inotropy.

Indirect effects: metabolic byproduct accumulation causing peripheral vasodilation.

Myeloproliferative Disorders:

High cell turnover and increased oxygen consumption drive compensatory CO increase.

Sepsis (Hyperdynamic Phase):

Cytokine-mediated global vasodilation.

Note: Often transient; may transition to sepsis-induced myocardial depression.

Category B: Peripheral Vascular Effects (Shunting/Vasodilation)

Arteriovenous Fistulas (AVF) / Malformations (AVM):

Most Common Cause: Iatrogenic AVF for Hemodialysis (ESRD population).

Bypasses high-resistance capillary beds, dumping arterial blood directly into venous circulation.

Chronic Liver Disease (Cirrhosis):

Formation of “spider angiomata” and internal AV shunts.

Impaired clearance of endogenous vasodilators (e.g., Nitric Oxide).

Thiamine Deficiency (Wet Beriberi):

Accumulation of pyruvate/lactate → systemic vasodilation.

Histopathology: Vacuolation, myofiber hypertrophy, and interstitial edema.

Chronic Lung Disease:

Hypoxia/Hypercapnia-driven systemic vasodilation.

Concomitant pulmonary HTN (RV remodeling) but preserved/high LV output.

Others: Paget’s disease of bone (extensive micro-shunting), Carcinoid syndrome, Mitochondrial diseases, Acromegaly, Erythroderma.

4. Special Focus: Hemodialysis Access-Induced HOHF

Physiologic Phases of AVF Creation:

Acute Phase:

Immediate ↓ SVR.

↑ Stroke volume and Heart Rate (SNS-mediated).

Endothelial shear stress → Nitric Oxide release → further arterial dilation.

Subacute Phase (Days to 2 Weeks):

RAAS-driven volume expansion.

↑ Right Atrial, Pulmonary Artery, and LV End-Diastolic Pressures (LVEDP).

Natriuretic peptide surge (BNP/ANP) peaks around Day 10.

Chronic Phase (Weeks to Months):

Adaptive hypertrophy.

Decompensation occurs when dilation exceeds contractility limits.

5. Point-of-Care