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**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

---

1. Core Definition & Hemodynamic Profile Clinical Paradox:* Congestive symptoms (pulmonary edema, JVD, peripheral edema) in the setting of a hyperdynamic, supranormal cardiac function.

2. 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.

3. Pathophysiology: The Hemodynamic Paradox Primary Insult:* Decreased SVR (either via peripheral vasodilation or arteriovenous shunting).

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

5. 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.

---

1. 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 angiomataR...