Episode 221: High-Output Heart Failure

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Mar 24, 2026

Nicolas Gonzalez, MD, an emergency physician and chief resident, walks through high-output heart failure basics and bedside clues. He explains pathophysiology, causes like AV fistulas and thyrotoxicosis, practical exam and POCUS findings, and pragmatic ED management including when to target access flow. Short, clinical, and focused on what to look for and how to act.

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ANECDOTE

Dialysis Patient Who's Wet But Warm

A dialysis patient can present profoundly volume overloaded yet warm and well perfused despite recent hemodialysis.
Nicolas Gonzalez describes an ESRD patient post-dialysis with JVD, pulmonary rales, pitting edema, bounding pulses, and elevated BNP and troponin.

INSIGHT

Hemodynamic Paradox Of High Output Heart Failure

High-output heart failure is defined by supranormal cardiac output with pathologically low systemic vascular resistance.
Nicolas Gonzalez states criteria: cardiac index >4 L/min/m2 or CO >8 L/min producing effective arterial underfilling and neurohormonal volume retention.

INSIGHT

Two Buckets Of Causes

Etiologies split into increased metabolic demand versus peripheral vascular changes that lower SVR.
Nicolas Gonzalez highlights hyperthyroidism and myeloproliferative disorders as metabolic drivers that increase tissue metabolism and reduce SVR.

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

Hosts:
Nicolas Gonzalez, MD
Brian Gilberti, MD

Download Leave a Comment 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): $> 4.0 L/min/m^{2}$ .
- 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 $\to$ eccentric remodeling $\to$ chamber dilation $\to$ 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 $\to$ 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:
1. Immediate $↓$ SVR.
2. $↑$ Stroke volume and Heart Rate (SNS-mediated).
3. Endothelial shear stress $\to$ Nitric Oxide release $\to$ further arterial dilation.
Subacute Phase (Days to 2 Weeks):
1. RAAS-driven volume expansion.
2. $↑$ Right Atrial, Pulmonary Artery, and LV End-Diastolic Pressures (LVEDP).
3. Natriuretic peptide surge (BNP/ANP) peaks around Day 10.
Chronic Phase (Weeks to Months):
1. Adaptive hypertrophy.
2. Decompensation occurs when dilation exceeds contractility limits.

5. Point-of-Care Physical Exam & Maneuvers

Nicoladoni-Branham Sign (Pathognomonic for Shunt-driven HOHF):
- Maneuver: Manually compress the AVF (or inflate cuff to $> 50 mmHg$ above SBP) for 30 seconds.
- Positive Result: Reflexive bradycardia or a transient rise in systemic BP.
- Significance: Confirms the shunt is a major contributor to the cardiac workload.
Peripheral Pulse Assessment:
- Water Hammer Pulses: Rapid upstroke and collapse.
- Quincke’s Pulse: Visible capillary pulsations in the nail beds.
- Traube’s Sign: “Pistol-shot” sounds auscultated over the femoral arteries.
Volume Status: Rales, S3 gallop, peripheral edema (standard HF signs).

6. Diagnostic Workup (Technical Targets)

POCUS / Echocardiography:

Left Ventricle: Hyperdynamic function; EF typically $> 60%$ .
Left Atrium: Significant dilation (Left Atrial Volume Index $> 34 mL/m^{2}$ ; Case study noted $72 mL/m^{2}$ ).
IVC: Plethoric with minimal respiratory variation.
Doppler: High flow velocities across the AV access if applicable.

Laboratory Evaluation:

BNP/NT-proBNP: Often markedly elevated (e.g., $> 70, 000$ in severe cases), though mean values in literature hover around $700 - 800 pg/mL$ .
Hematology: CBC to evaluate for severe anemia (trigger for HOHF if $Hgb < 7 - 8 g/dL$ ) or myeloproliferative markers.
Endocrine/Metabolic: TSH (Thyrotoxicosis), Serum Thiamine (Beriberi), LFTs (Cirrhosis).

7. Management Strategy: A Stepwise Approach

Phase 1: Immediate Stabilization (Volume Offloading)

Diuresis: Aggressive IV loop diuretics (Bumetanide/Furosemide).
Ultrafiltration: Preferred in ESRD patients failing to respond to dialysis or with refractory congestion.
Vasodilator Caution: Avoid aggressive Nitroglycerin or ACE-inhibitors initially.
- Rationale: Baseline SVR is already pathologically low; further reduction may precipitate profound hypotension/circulatory collapse.

Phase 2: Targeted Therapy (Etiology Specific)

Anemia: Transfuse to goal $Hgb > 7 - 8 g/dL$ to reduce demand.
Beriberi: High-dose IV Thiamine ( $100 - 500 mg$ ).
Thyrotoxicosis: Beta-blockers (Propranolol) + Antithyroid meds (PTU/Methimazole).

Phase 3: Surgical/Interventional Salvage (Refractory AVF Cases)

Closure of Accessory Sites: If multiple fistulas exist, close the non-dominant/unused sites.
Flow Reduction (Banding): Surgical narrowing of the fistula to target flow $< 600 mL/min$ .
RUDI Procedure: Revision Using Distal Inflow (moving inflow to a smaller, more distal artery).
Ligation: Complete closure of the AVF.
- Note: Requires bridge to Tunneled Dialysis Catheter or AV graft (higher resistance than fistulas).

8. Key Clinical Takeaways

The “Normal EF” Trap: Do not be reassured by an EF of $55 - 65%$ ; in the context of pulmonary edema and high CO, this is potentially HOHF.
Pulse Pressure: Look for a wide pulse pressure (e.g., $180/60$ ) as a marker of low SVR.
ESRD Logic: If an ESRD patient is “wet” immediately after HD, the problem is likely flow (AVF), not just fluid.