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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:

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.

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.

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.

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.

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.

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).

Left Ventricle: Hyperdynamic function; EF typically >60%.

Left Atrium: Significant dilation (Left Atrial Volume Index >34 mL/m2; Case study noted 72 mL/m2).

IVC: Plethoric with minimal respiratory variation.

Doppler: High flow velocities across the AV access if applicable.

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).

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.

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).

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).

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.

The post PODCAST: High-Output Heart Failure first appeared on האיגוד הישראלי לרפואה דחופה.

In this episode, Sam Ashoo, MD and T.R. Eckler, MD discuss the February 2026 Emergency Medicine Practice article, Emergency Department Diagnosis and Management of Acute Coronary Occlusion

00:00 – Introduction & Welcome

01:21 – Episode Overview: Acute Coronary Occlusion

02:06 – Why This Topic Matters: Statistics & New Guidelines

03:35 – Nomenclature: ACO vs STEMI/NSTEMI

06:15 – Differential Diagnosis for STEMI

07:41 – Pre-Hospital Care & EMS Role

11:37 – Patient History & Presenting Symptoms

12:28 – Physical Examination Findings

14:54 – EKG: The Most Important Test

17:00 – STEMI Definition & Criteria

20:32 – STEMI Equivalents: Scarbosa Criteria

22:40 – Smith Modified Scarbosa Criteria

24:10 – Hyperacute T Waves

25:30 – Posterior STEMI

28:40 – De Winter Sign

29:38 – Non-STEMI EKG Findings

31:30 – AVR ST Elevation

32:47 – Wellens Syndrome

33:54 – Reciprocal ST Segment Changes

36:15 – Inferior MI Patterns

37:54 – Laboratory Testing

39:51 – Imaging: Chest X-Ray & Echocardiography

42:25 – Supplemental Oxygen: What the Evidence Shows

44:50 – Analgesia & Pain Management

46:35 – Pharmacotherapy: Aspirin & Antiplatelet Agents

49:18 – Reperfusion Therapies & Thrombolytics

53:05 – Cardiac Arrest in STEMI Patients

53:55 – Closing Remarks & CME Information

The post PODCAST: Acute Coronary Occlusion first appeared on האיגוד הישראלי לרפואה דחופה.