Podcasts · Core EM - Emergency Medicine Podcast
Episode 221: High-Output Heart Failure
· Episode 221
Episode 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
Download Leave a Comment Tags: Cardiology
Show Notes Core EM Modular CME Course
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Course Highlights:
• Credit: 12.5 AMA PRA Category 1 Credits™ • Curriculum: Comprehensive coverage of Core Emergency Medicine, with 12 modules spanning from Critical Care to Pediatrics. • Cost:
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Click Here to Register and Begin Module 1 1. Core Definition & Hemodynamic Profile
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Clinical Paradox: Congestive symptoms (pulmonary edema, JVD, peripheral edema) in the setting of a hyperdynamic, supranormal cardiac function.
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Hemodynamic Criteria:
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Cardiac Index (CI): >4.0 L/min/m2.
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Cardiac Output (CO): >8 L/min.
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Systemic Vascular Resistance (SVR): Pathologically low (vasodilated or shunted state).
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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
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Primary Insult: Decreased SVR (either via peripheral vasodilation or arteriovenous shunting).
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Effective Arterial Blood Volume: Paradoxically low despite high total CO.
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Neurohormonal Cascade:
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Activation of Renin-Angiotensin-Aldosterone System (RAAS).
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Increased Sympathetic Nervous System tone.
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Increased Antidiuretic Hormone (ADH) secretion.
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Resultant State: Avid renal salt and water retention leading to massive plasma volume expansion.
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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)
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Hyperthyroidism/Thyrotoxicosis:
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Direct T3 effects: increased chronotropy/inotropy.
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Indirect effects: metabolic byproduct accumulation causing peripheral vasodilation.
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Myeloproliferative Disorders:
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High cell turnover and increased oxygen consumption drive compensatory CO increase.
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Sepsis (Hyperdynamic Phase):
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Cytokine-mediated global vasodilation.
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Note: Often transient; may transition to sepsis-induced myocardial depression.
Category B: Peripheral Vascular Effects (Shunting/Vasodilation)
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Arteriovenous Fistulas (AVF) / Malformations (AVM):
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Most Common Cause: Iatrogenic AVF for Hemodialysis (ESRD population).
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Bypasses high-resistance capillary beds, dumping arterial blood directly into venous circulation.
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Chronic Liver Disease (Cirrhosis):
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Formation of “spider angiomata” and internal AV shunts.
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Impaired clearance of endogenous vasodilators (e.g., Nitric Oxide).
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Thiamine Deficiency (Wet Beriberi):
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Accumulation of pyruvate/lactate → systemic vasodilation.
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Histopathology: Vacuolation, myofiber hypertrophy, and interstitial edema.
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Chronic Lung Disease:
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Hypoxia/Hypercapnia-driven systemic vasodilation.
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Concomitant pulmonary HTN (RV remodeling) but preserved/high LV output.
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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:
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Acute Phase:
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Immediate ↓ SVR.
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↑ Stroke volume and Heart Rate (SNS-mediated).
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Endothelial shear stress → Nitric Oxide release → further arterial dilation.
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Subacute Phase (Days to 2 Weeks):
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RAAS-driven volume expansion.
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↑ Right Atrial, Pulmonary Artery, and LV End-Diastolic Pressures (LVEDP).
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Natriuretic peptide surge (BNP/ANP) peaks around Day 10.
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Chronic Phase…
Links in the notes 5
- https://coreem.net/podcast/episode-221-high-output-heart-failure/
- https://media.blubrry.com/coreem/content.blubrry.com/coreem/HOHF.mp3
- https://coreem.net/podcast/episode-221-high-output-heart-failure/#comments
- https://coreem.net/tag/cardiology/
- https://www.highmarksce.com/nyumc/Planners/viewActivity?style=2&preview=true&plannerID=3560#CourseDetails
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