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Core EM - Emergency Medicine Podcast

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by Core EM

4.6(302 reviews)

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Core EM Emergency Medicine Podcast

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Recent Episodes

May 15, 2026

Episode 223: Thyroid Storm

Annaliese Elam, MD, and Brian Gilberti, MD, discuss the diagnosis, workup, and four-step treatment protocol for thyroid storm, offering a clear management strategy.

April 7, 2026

Episode 222: Local Anesthetic Systemic Toxicity (LAST)

<div class="row"> <div class="col-sm-4"> <a href="https://coreem.net/podcast/episode-222-local-anesthetic-systemic-toxicity-last/" title="Episode 222: Local Anesthetic Systemic Toxicity (LAST)" rel="bookmark"> <img width="576" height="576" src="https://coreem.net/content/uploads/2026/04/LAST.001.jpeg" class="img-responsive wp-post-image" alt="" decoding="async" loading="lazy" srcset="https://i0.wp.com/coreem.net/content/uploads/2026/04/LAST.001.jpeg?w=576&ssl=1 576w, https://i0.wp.com/coreem.net/content/uploads/2026/04/LAST.001.jpeg?resize=300%2C300&ssl=1 300w, https://i0.wp.com/coreem.net/content/uploads/2026/04/LAST.001.jpeg?resize=150%2C150&ssl=1 150w, https://i0.wp.com/coreem.net/content/uploads/2026/04/LAST.001.jpeg?resize=500%2C500&ssl=1 500w" sizes="auto, (max-width: 576px) 100vw, 576px" title="" /> </a> </div> <div class="col-sm-8"> <div class="post-content"> We discuss this ominous complication of providing local anesthesia. Hosts: Elaine Jonas, MD Brian Gilberti, MD </div> <div class="audio-player"> <div class="player"> <audio class="wp-audio-shortcode" id="audio-13141-4" preload="none" style="width: 100%;" controls="controls"><source type="audio/mpeg" src="https://media.blubrry.com/coreem/content.blubrry.com/coreem/LAST.mp3?_=4" /><a href="https://media.blubrry.com/coreem/content.blubrry.com/coreem/LAST.mp3">https://media.blubrry.com/coreem/content.blubrry.com/coreem/LAST.mp3</a></audio> </div> </div> <a class="download" href="https://media.blubrry.com/coreem/content.blubrry.com/coreem/LAST.mp3" title="Download" download>Download</a> <a href="https://coreem.net/podcast/episode-222-local-anesthetic-systemic-toxicity-last/#comments">Leave a Comment</a> Tags: <a href="https://coreem.net/tag/critical-care/" rel="tag">Critical Care</a>, <a href="https://coreem.net/tag/toxicology/" rel="tag">Toxicology</a> </div> </div> <div class="row"> <div class="col-md-12 post-content"> <h2>Show Notes</h2> <h2 data-path-to-node="3">I. Pathophysiology & Mechanisms</h2> <ul data-path-to-node="4"> <li> Definition: Systemic toxicity secondary to local anesthetic (LA) via accidental intravascular injection or excessive systemic absorption. </li> <li> Threshold: Occurs when plasma concentration exceeds the safety threshold for cardiac and neural tissue. </li> <li> Agent Profile: Bupivacaine (High Risk) <ul data-path-to-node="4,2,1"> <li> Highly lipophilic with high protein binding. </li> <li> “Fast-on, Slow-off” Kinetics: Strong Na+ channel binding with extremely slow dissociation during diastole. </li> <li> Myocardial Depression: Direct inhibition of Ca2+ release from the sarcoplasmic reticulum, impairing contractility. </li> <li> Low CC:CNS Ratio: The dose required for cardiac collapse is very close to the dose that triggers seizures (narrow safety margin). </li> </ul> </li> <li> Contributing Factors: <ul data-path-to-node="4,3,1"> <li> Acidosis/Hypercapnia: Increases the fraction of free drug and promotes ion trapping in the brain/heart; shifts the LA-binding curve toward higher toxicity. </li> <li> Hypoxemia: Exacerbates myocardial depression and lowers seizure threshold. </li> </ul> </li> </ul> <hr data-path-to-node="5" /> <h2 data-path-to-node="6">II. Risk Assessment & Prevention</h2> <h3 data-path-to-node="7">Patient-Specific Risk Factors</h3> <ul data-path-to-node="8"> <li> Extremes of Age: Neonates (low α-1-acid glycoprotein) and elderly (reduced clearance). </li> <li> Body Composition: Low muscle mass/frailty (decreased volume of distribution). </li> <li> Organ Dysfunction: <ul data-path-to-node="8,2,1"> <li> Hepatic: Reduced metabolism of amide LAs. </li> <li> Renal: Accumulation of metabolites; risk of metabolic acidosis lowering seizure threshold. </li> <li> Cardiac: Reduced cardiac output slows hepatic delivery/clearance; heart failure patients are more sensitive to Na+ channel blockade. </li> </ul> </li> <li> Pregnancy: Increased sensitivity to cardiotoxicity. </li> </ul> <h3 data-path-to-node="9">Procedural Risk Factors</h3> <ul data-path-to-node="10"> <li> Vascularity of Site (Highest to Lowest Risk): <ol start="1" data-path-to-node="10,0,1"> <li> Intercostal blocks (highest absorption rate). </li> <li> Caudal/Epidural. </li> <li> Interfascial plane blocks (e.g., TAP block). </li> <li> Psoas compartment/Sciatic. </li> <li> Brachial plexus. </li> </ol> </li> <li> Technique: Large volume infiltration, lack of ultrasound, lack of incremental injection. </li> </ul> <h3 data-path-to-node="11">Prevention Mandates</h3> <ul data-path-to-node="12"> <li> Weight-Based Dosing: <ul data-path-to-node="12,0,1"> <li> Lidocaine (Plain): Max 4.5 mg/kg. </li> <li> Lidocaine (with Epi): Max 7 mg/kg. </li> <li> Bupivacaine: Max 2.5–3 mg/kg. </li> </ul> </li> <li> Incremental Injection: 3–5 mL aliquots with frequent aspiration. </li> <li> Intravascular Marker: Use Epinephrine (1:200,000) to detect accidental IV placement (HR increase 10\text{ bpm}" data-index-in-node="97">>10 bpmor SBP increase 15\text{ mmHg}" data-index-in-node="128">>15 mmHg). </li> </ul> <hr data-path-to-node="13" /> <h2 data-path-to-node="14">III. Clinical Presentation</h2> <h3 data-path-to-node="16">Neurologic Phase (Early to Late)</h3> <ul data-path-to-node="17"> <li> Subjective: Metallic taste, tinnitus, circumoral numbness/tingling. </li> <li> Objective: Visual disturbances, agitation, confusion, tremors. </li> <li> Critical: Generalized tonic-clonic seizures, rapid progression to CNS depression, coma, and apnea. </li> <li> Note: Early phases are often masked in patients receiving midazolam or propofol. </li> </ul> <h3 data-path-to-node="18">Cardiovascular Phase</h3> <ul data-path-to-node="19"> <li> Initial: Hypertension and tachycardia (if epi used) or transient stimulatory phase. </li> <li> Conduction Defects: PR prolongation, QRS widening (classic sign), bundle branch blocks. </li> <li> Dysrhythmias: Bradycardia (most common), VT/VF, PEA, asystole. </li> <li> Contractility: Profound, refractory hypotension and cardiogenic shock. </li> </ul> <hr data-path-to-node="20" /> <h2 data-path-to-node="21">IV. Immediate Management Algorithm</h2> Goal: Prevent hypoxia/acidosis and sequester the toxin. <h3 data-path-to-node="23">1. Initial Actions</h3> <ul data-path-to-node="24"> <li> Stop Injection: Immediately halt all LA administration. </li> <li> Call for Help: Specify “LAST Protocol” and “Intralipid Kit.” </li> <li> Airway Management: <ul data-path-to-node="24"> <li> 100% O2. </li> <li> Hyperventilate slightly if needed to counter respiratory acidosis. </li> <li> Low threshold for intubation (hypoxia/acidosis rapidly worsen LAST). </li> </ul> </li> </ul> <h3 data-path-to-node="25">2. Seizure Control</h3> <ul data-path-to-node="26"> <li> First-line: Benzodiazepines (e.g., Midazolam). </li> <li> Avoid: Propofol if hemodynamically unstable (exacerbates cardiac depression). </li> <li> Neuromuscular Blockers: May be needed for ventilation, but remember they do not stop CNS seizure activity. </li> </ul> <h3 data-path-to-node="27">3. Lipid Emulsion Therapy 20%</h3> <ul data-path-to-node="28"> <li> Indications: Start at first sign of serious toxicity (airway compromise, seizures, or CV instability). </li> <li> Bolus: 1.5 mL/kg IV over 1 minute. </li> <li> Infusion: 0.25 mL/kg/min immediately following bolus. </li> <li> If Instability Persists: <ul data-path-to-node="28,3,1"> <li> Repeat bolus (up to 2 times). </li> <li> Increase infusion to 0.5 mL/kg/min. </li> </ul> </li> <li> Upper Limit: ≈12 mL/kg total dose. </li> </ul> <h3 data-path-to-node="29">4. Modified ACLS</h3> <ul data-path-to-node="30"> <li> Epinephrine: Use low doses (<1 mcg/kg) to avoid worsening arrhythmias and interfering with lipid rescue. </li> <li> Antiarrhythmics: Amiodarone is preferred. </li> <li> CONTRAINDICATED: <ul data-path-to-node="30,2,1"> <li> Lidocaine: (Class Ib antiarrhythmic—will worsen toxicity). </li> <li> Vasopressin: Associated with poor outcomes in animal LAST models. </li> <li> Calcium Channel Blockers / Beta Blockers: Exacerbate myocardial depression. </li> </ul> </li> <li> Refractory Arrest: Early consultation for ECMO or Cardiopulmonary Bypass (CPB). </li> </ul> <hr data-path-to-node="31" /> <h2 data-path-to-node="32">V. Differential Diagnosis for the Peri-Procedural Patient</h2> <ul data-path-to-node="33"> <li> High Spinal: Ascending sensory/motor block, profound sympathectomy (hypotension/bradycardia). </li> <li> Anaphylaxis: Urticaria, wheezing (rare with amides, more common with esters). </li> <li> Air/Gas Embolism: Sudden dyspnea, “mill-wheel” murmur, acute right heart strain. </li> <li> Vasovagal Syncope: Bradycardia/hypotension, usually lacks the QRS widening or seizure activity. </li> </ul> <hr data-path-to-node="34" /> <h2 data-path-to-node="35">VI. Post-Resuscitation & Complications</h2> <ul data-path-to-node="36"> <li> Observation: <ul data-path-to-node="36"> <li> At least 2 hours after a CNS-only event. </li> <li> At least 4–6 hours after a CV event. </li> </ul> </li> <li> Lipid Complications: <ul data-path-to-node="36,1,1"> <li> Lab Interference: Lipemia interferes with hemoglobin, creatinine, and electrolyte measurements (draw labs before ILE if possible). </li> <li> Pancreatitis: Rare, delayed complication of high-dose ILE. </li> <li> Fat Embolism/Overload: Rare pulmonary complications. </li> </ul> </li> </ul> <hr data-path-to-node="37" /> <h2 data-path-to-node="38">VII. Clinical “Red Flags” for Toxicity</h2> <ul data-path-to-node="39"> <li> Unexpected Agitation: In a patient who just received a block, don’t assume “anxiety.” </li> <li> Wide QRS: Any widening of the QRS complex post-injection is LAST until proven otherwise. </li> <li> Refractory Arrest: Standard ACLS failing in a patient who received LA. Lipid must be given. </li> </ul> <hr data-path-to-node="40" /> <blockquote data-path-to-node="41"> Critical Note: LAST is a clinical diagnosis. Do not wait for serum lidocaine levels or laboratory confirmation to initiate Lipid Emulsion Therapy. Immediate correction of pH and PaCO2 is as vital as the lipid itself. </blockquote> </div> </div> <a href="https://coreem.net/podcast/episode-222-local-anesthetic-systemic-toxicity-last/">Read More</a>

March 24, 2026

Episode 221: High-Output Heart Failure

<div class="row"> <div class="col-sm-4"> <a href="https://coreem.net/podcast/episode-221-high-output-heart-failure/" title="Episode 221: High-Output Heart Failure" rel="bookmark"> <img width="576" height="576" src="https://coreem.net/content/uploads/2026/03/HOHF.001.jpeg" class="img-responsive wp-post-image" alt="" decoding="async" loading="lazy" srcset="https://i0.wp.com/coreem.net/content/uploads/2026/03/HOHF.001.jpeg?w=576&ssl=1 576w, https://i0.wp.com/coreem.net/content/uploads/2026/03/HOHF.001.jpeg?resize=300%2C300&ssl=1 300w, https://i0.wp.com/coreem.net/content/uploads/2026/03/HOHF.001.jpeg?resize=150%2C150&ssl=1 150w, https://i0.wp.com/coreem.net/content/uploads/2026/03/HOHF.001.jpeg?resize=500%2C500&ssl=1 500w" sizes="auto, (max-width: 576px) 100vw, 576px" title="" /> </a> </div> <div class="col-sm-8"> <div class="post-content"> We discuss the diagnosis and treatment of one of EM's paradoxes: High-Output Heart Failure. Hosts: Nicolas Gonzalez, MD Brian Gilberti, MD </div> <div class="audio-player"> <div class="player"> <audio class="wp-audio-shortcode" id="audio-13095-6" preload="none" style="width: 100%;" controls="controls"><source type="audio/mpeg" src="https://media.blubrry.com/coreem/content.blubrry.com/coreem/HOHF.mp3?_=6" /><a href="https://media.blubrry.com/coreem/content.blubrry.com/coreem/HOHF.mp3">https://media.blubrry.com/coreem/content.blubrry.com/coreem/HOHF.mp3</a></audio> </div> </div> <a class="download" href="https://media.blubrry.com/coreem/content.blubrry.com/coreem/HOHF.mp3" title="Download" download>Download</a> <a href="https://coreem.net/podcast/episode-221-high-output-heart-failure/#comments">Leave a Comment</a> Tags: <a href="https://coreem.net/tag/cardiology/" rel="tag">Cardiology</a> </div> </div> <div class="row"> <div class="col-md-12 post-content"> <h2>Show Notes</h2> <h2>Core EM Modular CME Course</h2> 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: <ul> <li style="font-weight: 400">Credit: 12.5 AMA PRA Category 1 Credits™</li> <li style="font-weight: 400">Curriculum: Comprehensive coverage of Core Emergency Medicine, with 12 modules spanning from Critical Care to Pediatrics.</li> <li style="font-weight: 400">Cost: <ul> <li style="font-weight: 400">Free for NYU Learners</li> <li style="font-weight: 400">$250 for Non-NYU Learners</li> </ul> </li> </ul> <h3><a href="https://www.highmarksce.com/nyumc/Planners/viewActivity?style=2&preview=true&plannerID=3560#CourseDetails">Click Here to Register and Begin Module 1</a></h3> <hr /> <h2 data-path-to-node="1">1. Core Definition & Hemodynamic Profile</h2> <ul data-path-to-node="2"> <li> Clinical Paradox: Congestive symptoms (pulmonary edema, JVD, peripheral edema) in the setting of a hyperdynamic, supranormal cardiac function. </li> <li> Hemodynamic Criteria: <ul data-path-to-node="2,1,1"> <li> Cardiac Index (CI): 4.0\text{ L/min/m}^2" data-index-in-node="20">>4.0 L/min/m2. </li> <li> Cardiac Output (CO): 8\text{ L/min}" data-index-in-node="21">>8 L/min. </li> <li> Systemic Vascular Resistance (SVR): Pathologically low (vasodilated or shunted state). </li> </ul> </li> <li> The “Warm” Phenotype: Unlike standard HFrEF/HFpEF (often “Cold and Wet”), HOHF presents as “Warm and Wet” due to low SVR and bounding pulses. </li> </ul> <h2 data-path-to-node="3">2. Pathophysiology: The Hemodynamic Paradox</h2> <ul data-path-to-node="4"> <li> Primary Insult: Decreased SVR (either via peripheral vasodilation or arteriovenous shunting). </li> <li> Effective Arterial Blood Volume: Paradoxically low despite high total CO. </li> <li> Neurohormonal Cascade: <ul data-path-to-node="4"> <li> Activation of Renin-Angiotensin-Aldosterone System (RAAS). </li> <li> Increased Sympathetic Nervous System tone. </li> <li> Increased Antidiuretic Hormone (ADH) secretion. </li> </ul> </li> <li> Resultant State: Avid renal salt and water retention leading to massive plasma volume expansion. </li> <li> Cardiac Response: Chronic volume overload → eccentric remodeling → chamber dilation → eventual secondary myocardial failure/dilated cardiomyopathy. </li> </ul> <hr data-path-to-node="5" /> <h2 data-path-to-node="6">3. Differential Diagnosis: Etiological “Buckets”</h2> <h3 data-path-to-node="7">Category A: Increased Metabolic Demand (Systemic)</h3> <ul data-path-to-node="8"> <li> Hyperthyroidism/Thyrotoxicosis: <ul data-path-to-node="8"> <li> Direct T3 effects: increased chronotropy/inotropy. </li> <li> Indirect effects: metabolic byproduct accumulation causing peripheral vasodilation. </li> </ul> </li> <li> Myeloproliferative Disorders: <ul data-path-to-node="8"> <li> High cell turnover and increased oxygen consumption drive compensatory CO increase. </li> </ul> </li> <li> Sepsis (Hyperdynamic Phase): <ul data-path-to-node="8"> <li> Cytokine-mediated global vasodilation. </li> <li> Note: Often transient; may transition to sepsis-induced myocardial depression. </li> </ul> </li> </ul> <h4 data-path-to-node="9">Category B: Peripheral Vascular Effects (Shunting/Vasodilation)</h4> <ul data-path-to-node="10"> <li> Arteriovenous Fistulas (AVF) / Malformations (AVM): <ul data-path-to-node="10,0,1"> <li> Most Common Cause: Iatrogenic AVF for Hemodialysis (ESRD population). </li> <li> Bypasses high-resistance capillary beds, dumping arterial blood directly into venous circulation. </li> </ul> </li> <li> Chronic Liver Disease (Cirrhosis): <ul data-path-to-node="10"> <li> Formation of “spider angiomata” and internal AV shunts. </li> <li> Impaired clearance of endogenous vasodilators (e.g., Nitric Oxide). </li> </ul> </li> <li> Thiamine Deficiency (Wet Beriberi): <ul data-path-to-node="10"> <li> Accumulation of pyruvate/lactate → systemic vasodilation. </li> <li> Histopathology: Vacuolation, myofiber hypertrophy, and interstitial edema. </li> </ul> </li> <li> Chronic Lung Disease: <ul data-path-to-node="10"> <li> Hypoxia/Hypercapnia-driven systemic vasodilation. </li> <li> Concomitant pulmonary HTN (RV remodeling) but preserved/high LV output. </li> </ul> </li> <li> Others: Paget’s disease of bone (extensive micro-shunting), Carcinoid syndrome, Mitochondrial diseases, Acromegaly, Erythroderma. </li> </ul> <hr data-path-to-node="11" /> <h2 data-path-to-node="12">4. Special Focus: Hemodialysis Access-Induced HOHF</h2> <h3 data-path-to-node="13">Physiologic Phases of AVF Creation:</h3> <ol start="1" data-path-to-node="14"> <li> Acute Phase: <ol start="1" data-path-to-node="14"> <li> Immediate ↓ SVR. </li> <li> ↑ Stroke volume and Heart Rate (SNS-mediated). </li> <li> Endothelial shear stress → Nitric Oxide release → further arterial dilation. </li> </ol> </li> <li> Subacute Phase (Days to 2 Weeks): <ol start="1" data-path-to-node="14"> <li> RAAS-driven volume expansion. </li> <li> ↑ Right Atrial, Pulmonary Artery, and LV End-Diastolic Pressures (LVEDP). </li> <li> Natriuretic peptide surge (BNP/ANP) peaks around Day 10. </li> </ol> </li> <li> Chronic Phase (Weeks to Months): <ol start="1" data-path-to-node="14"> <li> Adaptive hypertrophy. </li> <li> Decompensation occurs when dilation exceeds contractility limits. </li> </ol> </li> </ol> <hr data-path-to-node="15" /> <h2 data-path-to-node="16">5. Point-of-Care Physical Exam & Maneuvers</h2> <ul data-path-to-node="17"> <li> Nicoladoni-Branham Sign (Pathognomonic for Shunt-driven HOHF): <ul data-path-to-node="17,0,1"> <li> Maneuver: Manually compress the AVF (or inflate cuff to 50\text{ mmHg}" data-index-in-node="56">>50 mmHg above SBP) for 30 seconds. </li> <li> Positive Result: Reflexive bradycardia or a transient rise in systemic BP. </li> <li> Significance: Confirms the shunt is a major contributor to the cardiac workload. </li> </ul> </li> <li> Peripheral Pulse Assessment: <ul data-path-to-node="17,1,1"> <li> Water Hammer Pulses: Rapid upstroke and collapse. </li> <li> Quincke’s Pulse: Visible capillary pulsations in the nail beds. </li> <li> Traube’s Sign: “Pistol-shot” sounds auscultated over the femoral arteries. </li> </ul> </li> <li> Volume Status: Rales, S3 gallop, peripheral edema (standard HF signs). </li> </ul> <hr data-path-to-node="18" /> <h2 data-path-to-node="19">6. Diagnostic Workup (Technical Targets)</h2> <h3 data-path-to-node="20">POCUS / Echocardiography:</h3> <ul data-path-to-node="21"> <li> Left Ventricle: Hyperdynamic function; EF typically 60\%" data-index-in-node="72">>60%. </li> <li> Left Atrium: Significant dilation (Left Atrial Volume Index 34\text{ mL/m}^2" data-index-in-node="60">>34 mL/m2; Case study noted 72 mL/m2). </li> <li> IVC: Plethoric with minimal respiratory variation. </li> <li> Doppler: High flow velocities across the AV access if applicable. </li> </ul> <h3 data-path-to-node="22">Laboratory Evaluation:</h3> <ul data-path-to-node="23"> <li> BNP/NT-proBNP: Often markedly elevated (e.g., 70,000" data-index-in-node="46">>70,000 in severe cases), though mean values in literature hover around 700–800 pg/mL. </li> <li> Hematology: CBC to evaluate for severe anemia (trigger for HOHF if Hgb<7–8 g/dL) or myeloproliferative markers. </li> <li> Endocrine/Metabolic: TSH (Thyrotoxicosis), Serum Thiamine (Beriberi), LFTs (Cirrhosis). </li> </ul> <hr data-path-to-node="24" /> <h2 data-path-to-node="25">7. Management Strategy: A Stepwise Approach</h2> <h3 data-path-to-node="26">Phase 1: Immediate Stabilization (Volume Offloading)</h3> <ul data-path-to-node="27"> <li> Diuresis: Aggressive IV loop diuretics (Bumetanide/Furosemide). </li> <li> Ultrafiltration: Preferred in ESRD patients failing to respond to dialysis or with refractory congestion. </li> <li> Vasodilator Caution: Avoid aggressive Nitroglycerin or ACE-inhibitors initially. <ul data-path-to-node="27,2,1"> <li> Rationale: Baseline SVR is already pathologically low; further reduction may precipitate profound hypotension/circulatory collapse. </li> </ul> </li> </ul> <h3 data-path-to-node="28">Phase 2: Targeted Therapy (Etiology Specific)</h3> <ul data-path-to-node="29"> <li> Anemia: Transfuse to goal 7\text{--}8\text{ g/dL}" data-index-in-node="26">Hgb>7–8 g/dL to reduce demand. </li> <li> Beriberi: High-dose IV Thiamine (100–500 mg). </li> <li> Thyrotoxicosis: Beta-blockers (Propranolol) + Antithyroid meds (PTU/Methimazole). </li> </ul> <h3 data-path-to-node="30">Phase 3: Surgical/Interventional Salvage (Refractory AVF Cases)</h3> <ol start="1" data-path-to-node="31"> <li> Closure of Accessory Sites: If multiple fistulas exist, close the non-dominant/unused sites. </li> <li> Flow Reduction (Banding): Surgical narrowing of the fistula to target flow <600 mL/min. </li> <li> RUDI Procedure: Revision Using Distal Inflow (moving inflow to a smaller, more distal artery). </li> <li> Ligation: Complete closure of the AVF. <ul data-path-to-node="31,3,1"> <li> Note: Requires bridge to Tunneled Dialysis Catheter or AV graft (higher resistance than fistulas). </li> </ul> </li> </ol> <hr data-path-to-node="32" /> <h2 data-path-to-node="33">8. Key Clinical Takeaways</h2> <ul data-path-to-node="34"> <li> 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. </li> <li> Pulse Pressure: Look for a wide pulse pressure (e.g., 180/60) as a marker of low SVR. </li> <li> ESRD Logic: If an ESRD patient is “wet” immediately after HD, the problem is likely flow (AVF), not just fluid. </li> </ul> </div> </div> <a href="https://coreem.net/podcast/episode-221-high-output-heart-failure/">Read More</a>

229 total episodes available with 29 transcripts

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