Episode 221: High-Output Heart Failure

(https://coreem.net/podcast/episode-22...) 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/cont... Download (https://media.blubrry.com/coreem/cont...) Leave a Comment (https://coreem.net/podcast/episode-22...) Tags: Cardiology (https://coreem.net/tag/cardiology/) Show Notes Core EM Modular CME Course Maximize your commute with the new Core EM Modular CME Course, featuring the most essential content distilled from our top-rated podcast episodes. This course offers 12 audio-based modules packed with pearls! Information and link below.  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: • Free for NYU Learners • $250 for Non-NYU Learners Click Here to Register and Begin Module 1 (https://www.highmarksce.com/nyumc/Pla...) 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 ...