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Core EM - Emergency Medicine Podcast

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Core EM - Emergency Medicine Podcast
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  • Core EM - Emergency Medicine Podcast

    Episode 218: Sympathetic Crashing Acute Pulmonary Edema (SCAPE)

    17/1/2026 | 12 min
    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





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    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.





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  • Core EM - Emergency Medicine Podcast

    Episode 217: Prehospital Blood Transfusion

    01/1/2026
    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





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    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





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  • Core EM - Emergency Medicine Podcast

    Episode 216: BRUE (Brief Resolved Unexplained Event)

    01/12/2025
    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





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    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.





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  • Core EM - Emergency Medicine Podcast

    Episode 215: Marburg Virus and Global EM

    01/11/2025
    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





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    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.





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  • Core EM - Emergency Medicine Podcast

    Episode 214: Acute Pulmonary Embolism

    02/10/2025
    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





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    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.





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