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 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. 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 (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. 4. Special Focus: Hemodialysis Access-Induced HOHF Physiologic Phases of AVF Creation: 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. 5. Point-of-Care Physical Exam & Maneuvers 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). 6. Diagnostic Workup (Technical Targets) POCUS / Echocardiography: 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. Laboratory Evaluation: 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). 7. Management Strategy: A Stepwise Approach Phase 1: Immediate Stabilization (Volume Offloading) 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. Phase 2: Targeted Therapy (Etiology Specific) 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). Phase 3: Surgical/Interventional Salvage (Refractory AVF Cases) 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). 8. Key Clinical Takeaways 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. Read More

We explore how to refine and optimize care in the vital minutes following ROSC. Hosts: Jonathan Elmer, MD, MS Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Post-ROSC_care.mp3 Download Leave a Comment 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 I. Phase 1: Stabilization (Minutes 0–10) The “Rearrest” Window & Pathophysiology High-Risk Period: Rearrest rates reach 30% within the first minutes post-ROSC. Shock Incidence: Two-thirds of patients develop profound hypotension/shock as initial resuscitative efforts subside. Catecholamine Washout: Super-physiologic “code-dose” epinephrine (1mg IV) typically wears off within ~3 minutes post-ROSC, leading to predictable hemodynamic collapse. Secondary Injuries: Evaluate for “CPR-induced trauma” (blunt thoracic trauma, rib fractures, pneumothorax, liver/splenic lacerations). Immediate Resuscitative Actions Vascular Access: Transition rapidly from IO to reliable IV access within 1–2 minutes. Prioritize Intraosseous (IO) placement within 5 minutes if IV attempts fail; intra-arrest data suggests no significant difference in early outcomes. Vasoactive “Bridge”: Maintain a “bolus-dose” pressor at the bedside for immediate push-dose titration. Options: Phenylephrine, dilute Epinephrine, or dilute Norepinephrine (titrated to effect rather than rigid dosing). Physician-Specific Task: Arterial Line: Goal: Placement within 5 minutes of ROSC. Preferred Site: Femoral (by landmarks/blind if necessary) for speed; should be a <2-minute procedure. Utility: Immediate detection of rearrest and beat-to-beat titration of vasopressors. II. Phase 2: Diagnostic Workup (Minutes 10–40) Etiology Epidemiology ACS Shift: Acute Coronary Syndrome (ACS) is the cause in only 6–10% of resuscitated survivors (lower than historical estimates). Common Etiologies: Respiratory: COPD, pneumonia, mucus plugging. Cardiac: Arrhythmia (cardiomyopathy/scar), RV failure (PE), or LV failure. Neurological: Intracranial hemorrhage (SAH/ICH), status epilepticus (4–5%). Metabolic: Dialysis-related disarray/hyperkalemia. Toxicology: Overdose accounts for ~10% of cases in urban centers. The “Broad Net” Strategy “Rainbow Labs”: Comprehensive panel including toxicology and serial biomarkers. Pan-Scan Protocol: Components: CT/CTA Head/Neck, Contrast CT Chest/Abdomen/Pelvis. Diagnostic Yield: 50% for clinically significant findings (causes or consequences of arrest). Contrast Risk: Negligible (1–2% increase in AKI risk) compared to the high diagnostic utility. Avoid Anchoring: Do not assume ischemic EKG changes are the cause; they are frequently a consequence of the global arrest-induced ischemia. III. Hemodynamic & Respiratory Targets Mean Arterial Pressure (MAP) Autoregulation Shift: In acute brain injury/post-arrest, the lower limit of cerebral autoregulation shifts right, often requiring MAPs of 110–120 mmHg for adequate perfusion. Clinical Target: Aim for MAP >80 mmHg. The BOX Trial Nuance: While the BOX trial showed no difference between MAP 63 vs. 77, its cohort (Denmark) had exceptionally high survival rates (70% back to work) and short response times, which may not generalize to North American populations with lower shockable rhythm incidence. Permissive Hypertension: If the patient is “self-driving” to higher pressures, do not aggressively lower them, as this may be a physiologic demand for cerebral blood flow. Ventilation and Oxygenation PaCO2 Management: Target: High-normal to slightly hypercarbic (45–55 mmHg). Rationale: Avoid accidental hyperventilation (PaCO2 <30), which can cut cerebral blood flow by 50%. PaO2 Management: Maintain normoxia; avoid extreme hyperoxia, though trial data (BOX trial) suggests small variances (70 vs 90 mmHg) are likely neutral. IV. Neurological Prognostication & Communication The “Stunned” Brain Anoxic Depolarization: Occurs within ~2 minutes of pulselessness as ATP-dependent ion pumps fail. Clinical Pitfall: Early neurological exams (absent pupils, no motor response) are unreliable in the first hours as they reflect global neuronal “stunning” rather than definitive permanent injury. Time Horizon: Meaningful recovery is measured in days/weeks, not minutes/hours. Family Engagement Presence: Bring family to the bedside immediately, including during procedures or continued resuscitation. Psychological Impact: Significantly reduces PTSD, anxiety, and depression in survivors’ families. Prognostic Honesty: Explicitly state “I don’t know” regarding etiology and outcome. Framing: Define “No News” as the best possible early outcome (preventing rearrest and stabilization). Read More

We review diagnosing and managing bacterial meningitis in the ED. Hosts: Sarah Fetterolf, MD Avir Mitra, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Meningitis_2_0.mp3 Download Leave a Comment Tags: CNS Infections, Infectious Diseases, Neurology 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 Patient Presentation & Workup Patient: 36-year-old male, currently shelter-domiciled, presenting with 3 weeks of generalized weakness, fevers, weight loss, and headaches. Vitals (Initial): BP 147/98, HR 150s, Temp 100.2°F, RR 18, O2 99% RA. Clinical Evolution: Initial assessment noted cachexia and a large ventral hernia. Following initial workup, the patient became acutely altered (A&O x0) and febrile to 102.9°F. Physical Exam Findings: Brudzinski Sign: Positive (knees flexed upward upon passive neck flexion). Kernig Sign: Discussed as highly specific (resistance/pain during knee extension with hip flexed at 90°). Meningeal Triad: Fever, nuchal rigidity, and AMS (present in 40% of cases; 95% of patients have at least two of the four cardinal symptoms including headache). Imaging: Chest X-ray: Scattered opacities (pneumonia) and a small pneumothorax. CT Abdomen/Pelvis: Confirmed asplenia (secondary to 2011 GSW/exploratory laparotomy). Head CT: Ventricle enlargement concerning for obstructive hydrocephalus and diffuse sulcal effacement. CSF Analysis & Microbiology Bacterial Meningitis Opening Pressure: Elevated (Normal is <170 mm H2​O). Color: Cloudy or turbid. Gram Stain: Positive in 60%–80% of cases before antibiotics; drops to 7%–41% after antibiotics. Cell Count: Very high (>1000–2000/mm3 WBC); dominated by neutrophils (>80% PMN). Glucose: Low (<40 mg/dL); CSF/blood glucose ratio is <0.3–0.4. Protein: High (>200 mg/dL). Cytology: Negative. Viral Meningitis Opening Pressure: Normal. Color: Clear or bloody. Gram Stain: Negative. Cell Count: Slightly elevated (<300/mm3 WBC); dominated by lymphocytes (<20% PMN). Glucose: Normal. Protein: Moderately elevated (<200 mg/dL). Cytology: Negative. Fungal Meningitis Opening Pressure: Normal to elevated. Color: Clear or cloudy. Gram Stain: Negative. Cell Count: Elevated (<500/mm3 WBC). Glucose: Normal to slightly low. Protein: High (>200 mg/dL). Cytology: Negative. Neoplastic (Cancer-related) Meningitis Opening Pressure: Normal. Color: Clear or cloudy. Gram Stain: Negative. Cell Count: Elevated (<300/mm3 WBC). Glucose: Normal to slightly low. Protein: High (>200 mg/dL). Cytology: Positive (this is the key differentiator). Management Protocol Immediate Treatment: Early administration of antibiotics/antivirals is critical to reduce mortality. Antibiotics: Ceftriaxone 2g IV q12h + Vancomycin (or Rifampin in cephalosporin-resistant areas). Listeria Coverage: Add Ampicillin for patients > 50 years old. Antivirals: Acyclovir 10 mg/kg q8h. Steroids: Dexamethasone 10 mg IV q6h for 4 days (proven to reduce mortality and improve outcomes). Surgical Intervention: Neurosurgery performed an emergent EVD in the ED to relieve pressure from obstructive hydrocephalus. Post-Exposure Prophylaxis: Indicated only for N. meningitidis (not S. pneumoniae) for contacts < 24 hours from diagnosis. Regimens: Rifampin for 2 days, single-dose Ciprofloxacin, or IM Ceftriaxone (if pregnant). Stats & Clinical Pearls: Austrian Syndrome The Triad: Concurrent pneumonia, endocarditis, and meningitis caused by Streptococcus pneumoniae. Risk Factors: Asplenia (due to the spleen’s role in filtering encapsulated bacteria), alcohol use disorder, and immunosuppression. Mortality Rate: Extremely high at 28%; mortality is highest when there is CNS involvement. Incidence: Worldwide, S. pneumoniae is the leading cause of bacterial meningitis, accounting for 3,000–6,000 cases annually. Read More

We discuss the diagnosis and management of SCAPE in the ED. Hosts: Naz Sarpoulaki, MD, MPH Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/SCAPEv2.mp3 Download Leave a Comment Tags: Acute Pulmonary Edema, Critical Care 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 The Clinical Case Presentation: 60-year-old male with a history of HTN and asthma. EMS Findings: Severe respiratory distress, SpO₂ in the 60s on NRB, HR 120, BP 230/180. Exam: Diaphoretic, diffuse crackles, warm extremities, pitting edema, and significant fatigue/work of breathing. Pre-hospital meds: NRB, Duonebs, Dexamethasone, and IM Epinephrine (under the assumption of severe asthma/anaphylaxis). Differential Diagnosis for the Hypoxic/Tachypneic Patient Pulmonary: Asthma/COPD, Pneumonia, ARDS, PE, Pneumothorax, Pulmonary Edema, ILD, Anaphylaxis. Cardiac: CHF, ACS, Tamponade. Systemic: Anemia, Acidosis. Neuro: Neuromuscular weakness. What is SCAPE? Sympathetic Crashing Acute Pulmonary Edema (SCAPE) is characterized by a sudden, massive sympathetic surge leading to intense vasoconstriction and a precipitous rise in afterload. Pathophysiology: Unlike HFrEF, these patients are often euvolemic or even hypovolemic. The primary issue is fluid maldistribution (fluid shifting from the vasculature into the lungs) due to extreme afterload. Bedside Diagnosis: POCUS vs. CXR POCUS is the gold standard for rapid bedside diagnosis. Lung Ultrasound: Look for diffuse B-lines (≥3 in ≥2 bilateral zones). Cardiac: Assess LV function and check for pericardial effusion. Why not CXR? A meta-analysis shows LUS has a sensitivity of ~88% and specificity of ~90%, whereas CXR sensitivity is only ~73%. Importantly, up to 20% of patients with decompensated HF will have a normal CXR. Management Strategy 1. NIPPV (CPAP or BiPAP) Start NIPPV immediately to reduce preload/afterload and recruit alveoli. Settings: CPAP 5–8 cm H₂O or BiPAP 10/5 cm H₂O. Escalate EPAP quickly but keep pressures to avoid gastric insufflation. Evidence: NIPPV reduces mortality (NNT 17) and intubation rates (NNT 13). 2. High-Dose Nitroglycerin The goal is to drop SBP to < 140–160 mmHg within minutes. No IV Access: 3–5 SL tabs (0.4 mg each) simultaneously. IV Bolus: 500–1000 mcg over 2 minutes. IV Infusion: Start at 100–200 mcg/min; titrate up rapidly (doses > 800 mcg/min may be required). Safety: ACEP policy supports high-dose NTG as both safe and effective for hypertensive HF. Use a dedicated line/short tubing to prevent adsorption issues. 3. Refractory Hypertension If SBP remains > 160 mmHg despite NIPPV and aggressive NTG, add a second vasodilator: Clevidipine: Ultra-short-acting calcium channel blocker (titratable and rapid). Nicardipine: Effective alternative for rapid BP control. Enalaprilat: Consider if the above are unavailable. Troubleshooting & Pitfalls The “Mask Intolerant” Patient Hypoxia is the primary driver of agitation. NIPPV is the best sedative. * Pharmacology: If needed, use small doses of benzodiazepines (Midazolam 0.5–1 mg IV). AVOID Morphine: Data suggests higher rates of adverse events, invasive ventilation, and mortality. A 2022 RCT was halted early due to harm in the morphine arm (43% adverse events vs. 18% with midazolam). The Role of Diuretics In SCAPE, diuretics are not first-line. The problem is redistribution, not volume excess. Diuretics will not help in the first 15–30 minutes and may worsen kidney function in a (relatively) hypovolemic patient. Delay Diuretics until the patient is stabilized and clear systemic volume overload (edema, weight gain) is confirmed. Disposition Admission: Typically requires CCU/ICU for ongoing NIPPV and titration of vasoactive infusions. Weaning: As BP normalizes and work of breathing improves, infusions and NIPPV can be gradually tapered. Take-Home Points Recognize SCAPE: Hyperacute dyspnea + severe HTN. Trust your POCUS (B-lines) over a “clear” CXR. NIPPV Immediately: Don’t wait. It saves lives and prevents tubes. High-Dose NTG: Use boluses to “catch up” to the sympathetic surge. Don’t fear the dose. Avoid Morphine: Use small doses of benzos if the patient is struggling with the mask. Lasix Later: Prioritize afterload reduction over diuresis in the hyperacute phase. Read More

We discuss the shift to prehospital blood to treat shock sooner. Hosts: Nichole Bosson, MD, MPH, FACEP Avir Mitra, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Prehospital_Transfusion.mp3 Download Leave a Comment Tags: EMS, Prehospital Care, Trauma 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 What is prehospital blood transfusion Administration of blood products in the field prior to hospital arrival Aimed at patients in hemorrhagic shock Why this matters Traditional US prehospital resuscitation relied on crystalloid ED and trauma care now prioritize early blood Hemorrhage occurs before hospital arrival Delays to definitive hemorrhage control are common Earlier blood may improve survival Supporting rationale ATLS and trauma paradigms emphasize blood over fluid National organizations support prehospital blood when feasible EMS already manages high risk, time sensitive interventions Evidence overview Data are mixed and evolving COMBAT: no benefit PAMPer: mortality benefit RePHILL: no clear benefit Signal toward benefit when transport time exceeds ~20 minutes Urban systems still experience long delays due to traffic and geography LA County median time to in hospital transfusion ~35 minutes LA County program ~2 years of planning before launch Pilot began April 1 Partnerships: LA County Fire Compton Fire Local trauma centers San Diego Blood Bank 14 units of blood circulating in the field Blood rotated back 14 days before expiration Ultimately used at Harbor UCLA Continuous temperature and safety monitoring Indications used in LA County Focused rollout Trauma related hemorrhagic shock Postpartum hemorrhage Physiologic criteria: SBP < 70 Or HR > 110 with SBP < 90 Shock index ≥ 1.2 Witnessed traumatic cardiac arrest Products: One unit whole blood preferred Two units PRBCs if whole blood unavailable Early experience ~28 patients transfused at time of discussion Evaluating: Indications Protocol adherence Time to transfusion Early outcomes Too early for outcome conclusions California collaboration Multiple active programs: Riverside (Corona Fire) LA County Ventura County Additional programs planned: Sacramento San Bernardino Programs meet monthly as CalDROP Focus on shared learning and operational optimization Barriers and concerns Trauma surgeon concerns about blood supply Need for system wide buy in Community engagement Patients who may decline transfusion Women of childbearing age and alloimmunization risk Risk of HDFN is extremely low Clear communication with receiving hospitals is essential Future direction Rapid national expansion expected Greatest benefit likely where transport delays exist Prehospital Blood Transfusion Coalition active nationally Major unresolved issue: reimbursement Currently funded largely by fire departments Sustainability depends on policy and payment reform Take-Home Points Hemorrhagic shock is best treated with blood, not crystalloid Prehospital transfusion may benefit patients with prolonged transport times Implementation requires strong partnerships with blood banks and trauma centers Early data are promising, but patient selection remains critical National collaboration is key to sustainability and future growth Read More

We review BRUEs (Brief Resolved Unexplained Events). Hosts: Ellen Duncan, MD, PhD Noumi Chowdhury, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/BRUE.mp3 Download Leave a Comment Tags: Pediatrics Show Notes What is a BRUE? BRUE stands for Brief Resolved Unexplained Event. It typically affects infants <1 year of age and is characterized by a sudden, brief, and now resolved episode of one or more of the following: Cyanosis or pallor Irregular, absent, or decreased breathing Marked change in tone (hypertonia or hypotonia) Altered level of responsiveness Crucial Caveat: BRUE is a diagnosis of exclusion. If the history and physical exam reveal a specific cause (e.g., reflux, seizure, infection), it is not a BRUE. Risk Stratification: Low Risk vs. High Risk Risk stratification is the most important step in management. While only 6-15% of cases meet strict “Low Risk” criteria, identifying these patients allows us to avoid unnecessary invasive testing. Low Risk Criteria To be considered Low Risk, the infant must meet ALL of the following: Age: > 60 days old Gestational Age: GA > 32 weeks (and Post-Conceptional Age > 45 weeks) Frequency: This is the first episode Duration: Lasted < 1 minute Intervention: No CPR performed by a trained professional Clinical Picture: Reassuring history and physical exam Management for Low Risk: Generally do not require extensive testing or admission. Prioritize safety education/anticipatory guidance. Ensure strict return precautions and close outpatient follow-up (within 24 hours). High Risk Criteria Any infant not meeting the low-risk criteria is automatically High Risk. Additional red flags include: Suspicion of child abuse History of toxin exposure Family history of sudden cardiac death Abnormal physical exam findings (trauma, neuro deficits) Management for High Risk: Requires a more thorough evaluation. Often requires hospital admission. Note: Serious underlying conditions are identified in approx. 4% of high-risk infants. Differential Diagnosis: “THE MISFITS” Mnemonic T – Trauma (Accidental or Non-accidental/Abuse) H – Heart (Congenital heart disease, dysrhythmias) E – Endocrine M – Metabolic (Inborn errors of metabolism) I – Infection (Sepsis, meningitis, pertussis, RSV) S – Seizures F – Formula (Reflux, allergy, aspiration) I – Intestinal Catastrophes (Volvulus, intussusception) T – Toxins (Medications, home exposures) S – Sepsis (Systemic infection) Workup & Diagnostics Step 1: Stabilization ABCs (Airway, Breathing, Circulation) Point-of-care Glucose Cardiorespiratory monitoring Step 2: Diagnostic Testing (For High Risk/Symptomatic Patients) Labs: VBG, CBC, Electrolytes. Imaging: CXR: Evaluate for infection and cardiothymic silhouette. EKG: Evaluate for QT prolongation or dysrhythmias. Neuro: Consider Head CT/MRI and EEG if there are concerns for trauma or seizures. Clinical Pearl: Only ~6% of diagnostic tests contribute meaningfully to the diagnosis. Be judicious—avoid “shotgunning” tests in low-risk patients. Prognosis & Outcomes Recurrence: Approximately 10% (lower than historical ALTE rates of 10-25%). Mortality: < 1%. Nearly always linked to an identifiable cause (abuse, metabolic disorder, severe infection). BRUE vs. SIDS: These are not the same. BRUE: Peaks < 2 months; occurs mostly during the day. SIDS: Peaks 2–4 months; occurs mostly midnight to 6:00 AM. Take-Home Points Diagnosis of Exclusion: You cannot call it a BRUE until you have ruled out obvious causes via history and physical. Strict Criteria: Stick strictly to the Low Risk criteria guidelines. If they miss even one (e.g., age < 60 days), they are High Risk. Education: For low-risk families, the most valuable intervention is reassurance, education, and arranging close follow-up. Systematic Approach: For high-risk infants, use a structured approach (like THE MISFITS) to ensure you don’t miss rare but reversible causes. Read More

Lessons from Rwanda’s Marburg Virus Outbreak and Building Resilient Systems in Global EM. Hosts: Tsion Firew, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Marburg_Virus.mp3 Download Leave a Comment Tags: Global Health, Infectious Diseases Show Notes Context and the Rwanda Marburg Experience The Threat: Marburg Virus Disease is from the same family as Ebola and has historically had a reported fatality rate as high as 90%. The Outbreak (Sept. 2024): Rwanda declared an MVD outbreak. The initial cases involved a miner, his pregnant wife (who fell ill and died after having a baby), and the baby (who also died). Healthcare Worker Impact: The wife was treated at an epicenter hospital. Eight HCWs were exposed to a nurse who was coding in the ICU; all eight developed symptoms, tested positive within a week, and four of them died. The Turning Point: The outbreak happened in city referral hospitals where advanced medical interventions (dialysis, mechanical ventilation) were available. Rapid Therapeutics Access: Within 10 days of identifying Marburg, novel therapies (experimental drugs and monoclonal antibodies) and an experimental vaccine were made available through diplomacy with the US government/CDC and agencies like WHO, Africa CDC, CEPI and more. The Outcome: This coordinated effort—combining therapeutics, widespread testing, and years of investment in a resilient healthcare system—helped curb the fatality rate down to 23%. Barriers and Enablers in Outbreak Preparedness Fragmented Systems: Emergency and surveillance functions often operate in silos, leading to delayed or missed outbreak identification (e.g., inconsistent travel screening at JFK during early COVID-19 vs. African countries). Solution: Empowering Emergency Departments and the community as the sentinel site can bridge this gap. Limited Frontline Capacity and Protection: Clinicians are often undertrained and underprotected and are frequently not part of the decision-making for surveillance. Weak Governance and Accountability: Unclear command structures and lack of feedback discourage early reporting. Enabler: Strong governance and accountability in Rwanda helped contain the virus. Dependence on External Programs: Many low-income countries rely on outside sources for vaccines and therapeutics, slowing response. Solution: Invest in local production (e.g., Rwanda’s pre-outbreak investment in developing its own mRNA vaccines). Lack of Resource-Smart Innovation: Gaps exist in things like integrating digital triage tools and surveillance systems. Four Pillars of a Responsive and Equitable Emergency System Workforce: Invest in pre-service and in-service training, mentorship, and fair compensation to ensure a skilled, protected, and motivated team. Integration into the Health System: Emergency care (including pre-hospital services) must not operate in silos; it needs to be embedded in national health strategies and linked to surveillance, referral, and financing systems. Equity in Design and Policy: The system must address the needs and protection of vulnerable groups and work closely with policymakers. Data: Utilize real-time data and dashboards to provide a feedback loop between clinicians and policymakers, enabling tailored and innovative interventions. Advice for Clinicians in Global Health Work Start Small and Build Trust: Meaningful work requires humility and relationship over scale or visibility. Focus on local priorities and sustainable change through long-term partnership, not just presence. Avoid the “savior mindset”. Be T-Shaped: Be deep in one specialty (e.g., EM) but fluent across other critical areas like policy, finance, and data, as these drive decision-making. Focus on Knowledge Transfer: True impact means making yourself less essential over time. Prioritize mentorship, co-creation, and sharing leadership opportunities. Looking Ahead: Global Threats Shaping the Next Decade The future of EM will be shaped by the convergence of several complex challenges: Climate and Environmental Crisis: Extreme heat, floods, and vector-borne illnesses will strain emergency systems. Preparation: Invest in climate-resilient infrastructure for both EDs and the community. Outbreaks and Biosecurity: Future outbreaks will emerge faster than current systems can handle, coupled with challenges from anti-microbial resistance. Conflict, Displacement, and Urbanization: Mass migration and overcrowded cities will require new models of emergency care that are mobile, scalable, and inclusive. Preparation: Building resilient healthcare systems ready for crisis mental health and cross-border coordination. Digital Tools and AI: These can augment solutions, but investment is needed in data governance and ethical AI that preserves local control and adapts to local capacity. Read More

We review the diagnosis, risk stratification, & management of acute pulmonary embolism in the ED. Hosts: Vivian Chiu, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Acute_Pulmonary_Embolism.mp3 Download One Comment Tags: Pulmonary Show Notes Core Concepts and Initial Approach Definition: Obstruction of pulmonary arteries, usually from a DVT in the proximal lower extremity veins (iliac/femoral), but may be tumor, air, or fat emboli. Incidence & Mortality: 300,000–370,000 cases/year in the USA, with 60,000–100,000 deaths annually. Mantra: “Don’t anchor on the obvious. Always risk stratify and resuscitate with precision.” Risk Factors: Broad, including older age, inherited thrombophilias, malignancy, recent surgery/trauma, travel, smoking, hormonal use, and pregnancy. Clinical Presentation and Risk Stratification Presentation: Highly variable, showing up as anything from subtle shortness of breath to collapse. Acute/Subacute: Dyspnea (most common), pleuritic chest pain, cough, hemoptysis, and syncope. Patients are likely tachycardic, tachypneic, hypoxemic on room air, and may have a low-grade fever. Chronic: Can mimic acute symptoms or be totally asymptomatic. Pulmonary Infarction Signs: Pleuritic pain, hemoptysis, and an effusion. High-Risk Red Flags: Signs of hypotension (systolic blood pressure < 90 mmHg for over 15 minutes), requirement of vasopressors, or signs of shock → activate PERT team immediately. Crucial Mimics: Think broadly; consider pneumonia, ACS, pneumothorax, heart failure exacerbation, and aortic dissection. Workup & Diagnostics History/Scoring: Ask about prior clots, recent surgeries, hospitalizations, travel. Use Wells/PERC criteria to assess pretest probability. Labs: D-dimer: A good test to rule out PE in a patient with low probability. If suspicion is high, proceed directly to imaging. Troponin/BNP: Act as RV stress gauges. Elevated levels are associated with increased risk of a complicated clinical course (25-40%). Lactate: Helpful in identifying patients in possible cardiogenic shock. EKG: Most common finding is sinus tachycardia. Classic RV strain patterns (S1Q3T3, T-wave changes/inversions) are nonspecific. Imaging: CXR: Usually normal, but quick and essential to rule out other causes. CTPA: The usual standard and gold standard for stable patients. High sensitivity (> 95%) and can detect RV enlargement/strain. V/Q Scan: Option for patients with contraindications to contrast (e.g., severe contrast allergies). POCUS (Point-of-Care Ultrasound): Useful adjunct for unstable patients. Bedside Echo: Can show signs of RV strain (enlarged RV, McConnell sign). Lower Extremity Ultrasound: Can identify a DVT in proximal leg veins. Treatment & Management Resuscitation (Reviving the RV): Oxygenation: Give supplementally as needed (nasal cannula, non-rebreather, high flow). Intubation: Avoid if possible; positive pressure ventilation can worsen RV dysfunction. Fluids: Be judicious; even the smallest amount can worsen RV overload. Vasopressors: Norepinephrine is preferred as first-line for hypotension/shock. Anticoagulation (Start Immediately): Initial choice is UFH or LMWH (Lovenox). Lovenox is preferred for quicker time to therapeutic range, but is contraindicated in renal dysfunction, older age, or need for emergent procedures. DOACs can be considered for stable, low-risk patients as an outpatient. Escalation for High-Risk PE Systemic Thrombolytics: Consider for very sick patients with shock/cardiac arrest (e.g., Alteplase 100 mg over two hours or a bolus in cardiac arrest). High risk of intracranial hemorrhage; weigh risks versus benefits. PERT Activation: Engage multidisciplinary teams (usually including ICU, CT surgery, and interventional radiology). Interventions: Consult specialists for catheter-directed thrombolysis or suction embolectomy. Surgical embolectomy can also be considered. Bridge to Care: Activate the ECMO team early for unstable patients to buy valuable time. Prognosis & Disposition Mortality: Low risk < 1%; intermediate 3-15%; high risk 25-65%. Complications: 3-4% of patients develop Chronic Thromboembolic Pulmonary Hypertension (CTEPH). Others may have long-term RV dysfunction and chronic shortness of breath. Recurrence: ∼ 30% chance in the next few weeks to months, if not treated correctly. Disposition: ICU: All high-risk and some intermediate-high risk patients. Regular Floor: Intermediate-low risk patients. Outpatient Discharge: Low-risk patients can be sent home on anticoagulation. Use PSI or HESTIA scores to risk stratify suitability, typically starting a DOAC. Shared Decision-Making: Critical to ensure care is safe and consistent with the patient’s wishes. Read More

We break down pneumothorax: risks, diagnosis, and management pearls. Hosts: Christopher Pham, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Pneumothorax.mp3 Download Leave a Comment Tags: Chest Trauma, Pulmonary, Trauma Show Notes Risk Factors for Pneumothorax Secondary pneumothorax Trauma: rib fractures, blunt chest trauma (as in the case). Iatrogenic: central line placement, thoracentesis, pleural procedures. Primary spontaneous pneumothorax Young, tall, thin males (10–30 years). Connective tissue disorders: Marfan, Ehlers-Danlos. Underlying lung disease: COPD with bullae, interstitial lung disease, CF, TB, malignancy. Technically, anyone is at risk. Symptoms & Differential Diagnosis Typical PTX presentation: Dyspnea, chest pain, pleuritic discomfort. Exam clues: unilateral decreased breath sounds, focal tenderness/crepitus. Red flags (suggest tension PTX): JVD Tracheal deviation Hypotension, shock physiology Severe tachycardia, hypoxia Differential diagnoses: Pulmonary: asthma, COPD, pneumonia, pulmonary edema (SCAPE), ILD, infections. Cardiac: ACS, CHF, pericarditis. PE and other acute causes of dyspnea. Diagnostics Bloodwork: limited role, except type & screen if intervention likely. EKG: reasonable given chest pain/shortness of breath. Imaging: POCUS (bedside ultrasound) High sensitivity (86–96%) & specificity (97–100%). Signs: Seashore sign: normal lung sliding. Barcode sign: absent lung sliding. Lung point: most specific for PTX. CXR Sensitivity ~70–90% for small PTX. May show pleural line, hyperlucency. CT chest (gold standard) Defines size/severity. Rules out mimics (bullae, pleural effusion, hemothorax). Guides intervention choice. Management First step for all: Oxygen supplementation (non-rebreather if possible). Accelerates resorption of pleural air. Stable vs. unstable decision point: Unstable/tension PTX Immediate needle thoracostomy (14-g angiocath, 2nd ICS midclavicular). Temporizing until chest tube/pigtail placed. Stable, small PTX (<2 cm on O₂) Observation, supplemental O₂, conservative management. Stable, larger PTX or symptomatic Chest tube or pigtail catheter insertion. Pigtail catheters: less invasive, more comfortable, similar efficacy for simple PTX. Large bore tubes: indicated if associated with blood, pus, large collections. Disposition Admit all patients with chest tubes; cannot be discharged with tube in place. Service responsible varies by hospital: trauma, CT surgery, MICU, etc. Level of care (ICU vs. floor) depends on stability: ICU if unstable course, intubated, shock physiology. Stepdown/floor if stable and straightforward. Take Home Points Always broaden differential in dyspnea/chest pain → don’t anchor on asthma/COPD. Exam findings + history (trauma, risk factors) crucial to raising suspicion. Ultrasound is more sensitive than CXR and highly specific when lung point found. Oxygen is first-line; intervention determined by size + stability. Pigtail catheters increasingly favored for simple, stable PTX. All patients with intervention require admission; service varies by institution. Read More

Angioedema – Recognition and Management in the ED Hosts: Maria Mulligan-Buckmiller, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Angioedema.mp3 Download Leave a Comment Tags: Airway Show Notes Definition & Pathophysiology Angioedema = localized swelling of mucous membranes and subcutaneous tissues due to increased vascular permeability. Triggers increased vascular permeability → fluid shifts into tissues. Etiologies Histamine-mediated (anaphylaxis) Associated with urticaria/hives, pruritus, and redness. Triggered by allergens (foods, insect stings, medications). Rapid onset (minutes to hours). Bradykinin-mediated Hereditary angioedema (HAE): C1 esterase inhibitor deficiency (autosomal dominant). Acquired angioedema: Associated with B-cell lymphoma, autoimmune disease, MGUS. Medication-induced: Most commonly ACE inhibitors; rarely ARBs. Typically lacks urticaria and itching. Gradual onset, can last days if untreated. Idiopathic angioedema Unknown cause; diagnosis of exclusion. Clinical Presentations Swelling Asymmetric, non-pitting, usually non-painful. May involve lips, tongue, face, extremities, GI tract. Respiratory compromise Upper airway swelling → stridor, dyspnea, sensation of throat closure. Airway obstruction is the most feared complication. Abdominal manifestations Bowel wall angioedema can mimic acute abdomen: Nausea, vomiting, diarrhea, severe pain, increased intra-abdominal pressure, possible ischemia. Key Differentiating Features Histamine-mediated: rapid onset, hives/itching, resolves quickly with epinephrine, antihistamines, and steroids. Bradykinin-mediated: slower onset, lacks urticaria, prolonged duration, less responsive to standard anaphylaxis medications. Diagnostic Approach in the ED Focus on airway (ABCs) and clinical assessment. Labs (e.g., C4 level) useful for downstream diagnosis (esp. HAE) but not for acute management. Imaging: only if symptoms suggest abdominal involvement or to rule out other causes. Treatment Strategies Airway protection is always priority: Early consideration of intubation if worsening obstruction or inability to manage secretions. Histamine-mediated (anaphylaxis): Epinephrine (IM), antihistamines, corticosteroids. Bradykinin-mediated: Epinephrine may be tried if unclear etiology (no significant harm, lifesaving if histamine-mediated). Targeted therapies: Icatibant: bradykinin receptor antagonist. Ecallantide: kallikrein inhibitor (less available). C1 esterase inhibitor concentrate: replenishes deficient protein. Fresh frozen plasma (FFP): contains C1 esterase inhibitor. Tranexamic acid (TXA): off-label, less evidence, considered if no other options. Complications to Watch For Airway compromise: rapid deterioration possible. Abdominal compartment syndrome from bowel edema (rare, surgical emergency). Take-Home Points Secure the airway if in doubt. Differentiate histamine-mediated vs bradykinin-mediated by presence/absence of hives/itching and speed of onset. Use epinephrine promptly if suspecting histamine-mediated angioedema or if uncertain. Consider bradykinin-targeted therapies for confirmed hereditary, acquired, or ACE-inhibitor–related angioedema. Recognize ACE inhibitors as the most frequent medication trigger; ARBs rarely cause it. Labs and imaging generally don’t change initial ED management but aid diagnosis for follow-up care. Read More