REBEL Cast

🧭 REBEL Rundown 🔑Key Points 🌱 Growth mindset transforms learning – Residents and students who believe skills can be developed are more open to feedback, more resilient after failure, and more engaged in practice.🧠 Language matters in feedback – Simple reframes such as “You’re developing procedural skills” instead of “You’re not strong at procedures” encourage persistence and normalize the learning curve.🤝 Mindset shapes team culture – Growth mindset leaders foster psychological safety, invite input, and create collaborative teams. Fixed mindset hierarchies, on the other hand, silence voices and can compromise patient care.🔥 Growth mindset protects against burnout – By reframing mistakes as part of the process, clinicians reduce perfectionism and shame, bolstering resilience and wellness.🔍 Practical steps start with self-talk – Add the word “yet” to limiting beliefs (“I’m not good at X…yet”) and shift feedback questions toward improvement (“What’s one thing I can do better next time?”).🛠️ Embracing mistakes with a growth mindset – Leads to more effective feedback loops and improvement do this by building a culture of psychological safety is crucial for growth and reducing medical errors. Click here for Direct Download of the Podcast. 👀Previously Covered and Related Content: REBEL EM: The EM MindsetREBEL EM: Titles Dont Make LeadersREBEL EM: Mind of the Resuscitationist with Scott WeingartEM Crit: Making Things Happen with Cliff Reid 📝 Introduction Welcome to this episode of REBEL MIND, where MIND stands for Mastering Internal Negativity during Difficulty. Here we sharpen the person behind the practitioner by focusing on things that improve our performance, optimizing team dynamics and the human behavior that embodies the hidden curriculum of medicine. Mindset shapes everything we do in medicine—from how we teach and learn to how we show up for patients at the bedside. Drawing from Carol Dweck’s influential book Mindset, this episode of REBEL MIND explores the critical difference between a fixed mindset (believing abilities are innate and static) and a growth mindset (seeing skills as things that can be developed through effort and feedback). We sat down with Dr. Kim Bambach, an emergency medicine physician and medical educator, and Dr. Frank Lodeserto, a dual-trained intensivist and internal medicine program director, to unpack how mindset influences medical education, bedside performance, and physician wellness. In this episode, we delve into how the mindset of clinicians can profoundly influence their performance, professional growth, and ultimately patient care Cognitive Question How does adopting a growth versus a fixed mindset influence clinical performance, medical education and patient outcomes? 🌱What is Growth vs Fixed Mindset? In Carol Dweck’s research, two primary mindsets are highlighted: Fixed mindset: Which sees intelligence and skills as staticIn the medical field, adopting a fixed mindset might lead a clinician to avoid complex cases due to fear of failure.Growth mindset: Which views abilities as improvable through dedication and effort. In contrast, a growth mindset encourages embracing challenges as opportunities for learning and development. 🏥How This Applies to the Emergency Department or ICU? In high-stakes environments like the ICU or the ED, the mindset adopted by healthcare providers can distinctly shape patient care and team dynamics. A fixed mindset might lead to defensive behaviors and a reluctance to engage in challenging cases, potentially stunting personal and professional growth. Conversely, a growth mindset not only fosters resilience and adaptability but also enhances team collaboration and patient outcomes by encouraging open communication, continuous learning, and acceptance of constructive feedback. ⏩Immediate Action Steps for Your Next Shift  **Monitor Self-Talk**: Notice your internal narrative when faced with challenges. Replace negative, fixed-mindset thoughts with growth-oriented ones like “Not yet” or “What can I learn from this?”**Promote a Culture of Inquiry**: Challenge yourself and your team to engage in constructive questioning and explore alternative diagnoses or treatment plans to encourage a growth-centered environment.**Model Vulnerability**: Share personal learning experiences and mistakes with colleagues to normalize the growth process and reduce the stigma of imperfection.**Reframe Feedback**: Instead of broadly asking, “How did I do?” inquire, “What’s one thing I can improve on next time?” This shift helps maintain focus on growth rather than performance validationFeedback is a whole another topic that we plan t

🧭 REBEL Rundown 🔑Key Points Try the coffee nap! Where you combine caffeine and a 30-minute nap to then have that boost energy and alertness by the time it kicks in.💤 Sleep isn’t optional—it’s crucial for memory, mood regulation, and physical recovery. It is fundamentally different from rest❌ Replacing sleep with caffeine isn’t effective and can have negative health impacts. Make getting enough sleep a priority🌞 Sunlight exposure is important for maintaining circadian rhythms and sleep quality. This applies even if you work as a nocturnist💡 Creating a personalized sleep system enhances quality and consistency. It gives you back control of a schedule that you may feel like is out of your hands.🧩 If you’ve tried these strategies and you’re still struggling, consider true sleep pathology (insomnia, shift work disorder, sleep apnea) and get help—this is not a “be tougher” problem.🩺 Better sleep isn’t just about feeling good; it’s directly tied to error reduction, patient safety, and longevity in EM/ICU careers. Click here for Direct Download of the Podcast. 👀Previously Covered and Related Content: REBEL Core Cast: Sleep HygieneREBEL MIND: Rest Is Not Sleep: The Seven Dimensions of True RecoveryRebellion in EM: Care For Yourself – Sleep HygieneFirst10EM: Some Evidence For Working Night ShiftsREBEL MIND: Dunning Kruger Effect 📝 Introduction Welcome to this episode of REBEL MIND, where MIND stands for Mastering Internal Negativity during Difficulty. Here we sharpen the person behind the practitioner by focusing on things that improve our performance, optimizing team dynamics and the human behavior that embodies the hidden curriculum of medicine. Today we are exploring the imperative topic of rest and why it’s not just about sleeping. The second of a two part series, hosted by Dr. Mark Ramzy with guests Dr. Maureen Aiad and Dr. Amil Badoolah, continue our discussion but this time on the multifaceted nature of sleep, how it serves as medicine and how we can use our tools deliberately to get more of it! Cognitive Question How would your clinical performance, patience with families, and long-term career sustainability change if you treated sleep as a non-negotiable clinical intervention rather than a flexible “nice-to-have”? 💤How is Sleep Different From Rest? 1. Rest reduces load; sleep repairs systemsWe previously talked about the 7 types of rest and you can check that out hereExamples of physical rest include: pausing tasks, stepping away from the monitor, taking a walk, stretching, breathing, journaling, connecting with a colleague. This lightens your cognitive/emotional burden.Sleep is fundamentally different in that it’s an active biologic process that helps:Consolidates memory and learning (yes, including the tough cases from last night).Regulates mood, impulse control, and emotional reactivity.Supports immunity, metabolic health, and cardiovascular function.Repairs tissue, replenishes neurotransmitters, and fine-tunes neural networks.You can have “rested but underslept” days (you took breaks but got 4 hours in bed), and “slept but unrested” days (you got hours, but all junk sleep). Both matter, but they are not interchangeable.2. Sleep architecture vs. “knocking out”True restorative sleep cycles through NREM and REM in predictable patterns.Alcohol, late caffeine, and fragmented nights may help you fall asleep faster but:Suppress REM.Shorten deep sleep.Increase awakenings and light sleep.The result: you technically slept, but your brain didn’t get the “software updates” it needed.Biology isn’t built for your scheduleCircadian rhythms were designed for light-day / dark-night cycles, not:10 pm–7 am ED shifts.24-hour calls.6 nights in a row followed by days.Your body can adapt partially, but not instantly and not perfectly. That’s why:You can feel “jet-lagged” even when you haven’t traveled.Sleep before and after nights feels odd and fragile.Recognizing that “this is biologically unnatural” is key: you’re not weak; you’re fighting physiology. 🏥How This Applies to the Emergency Department or ICU? Performance & safetySleep deprivation:Slows reaction time and increases error rate.Impairs risk assessment and complex decision-making.Drops your frustration tolerance with consultants, families, and staff.In both emergency medicine and critical care, that translates into:Anchoring on the wrong diagnosis.Missing subtle clinical changes.Snapping at a tech, nurse or resident and damaging team culture. Chronic health for chronic shift workLong-term sleep disruption is associated with:Hypertension, diabetes, obesity.Depression, anxiety, burnout.Arrhythmias (e.g., AFib) and increased stroke r

🧭 REBEL Rundown 📌 Key Points 🔍 Understanding the Why: The significance of understanding underlying causes, beyond initial diagnoses, in both sports and emergency medicine is explored. ⏱️ Recovery Focus: Emphasizing the importance of recovery time and small daily choices in optimizing performance for both athletes and emergency physicians. 📊 Data-Driven Insights: The Arena Labs approach uses personalized data, leveraging wearable technology and expert coaching to tackle burnout and enhance well-being. 🤝 Personalization and Partnership: Arena Labs’ collaboration with emergency clinicians sheds light on personalized performance solutions rooted in scientific evidence. Click here for Direct Download of the Podcast. 📝 Introduction Welcome back to REBEL MIND, where MIND stands for Mastering Internal Negativity during Difficulty. Here we sharpen the person behind the practitioner by focusing on things that improve our performance, optimizing team dynamics and the human behavior that embodies the hidden curriculum of medicine. In this episode, we’re excited to continue collaboration with Arena Labs, where host Dr. Mark Ramzy interviews Allyn Abadie, Arena Labs’ Principal Scientist on how we can apply performance science in and out of the emergency department. Arena Labs is helping us measure healthcare performance through innovative programs designed to combat burnout and enhance personal wellness using data-driven strategies. 🔙Previously Covered on REBEL MIND: Performance Under Pressure – What Medicine Can Learn from Elite TeamsThe Power of Performance Coaching in MedicineRest Is Not Sleep: The Seven Dimensions of True Recovery 🤔Cognitive Question How can emergency department clinicians utilize techniques inspired by athletic performance to better manage stress, prevent burnout, and optimize recovery? 💭 Why This is Important Burnout among healthcare workers is a growing concern, especially in such high-pressure environments as emergency and intensive care units. The collaboration with Arena Labs brings forth a vital focus on using data and coaching to build resilience among medical professionals. 🏥How This Applies to the Emergency Department or ICU? Emergency medicine, akin to high-performance sports, demands intense energy and quick decision-making under pressure, often leading to stress and burnout. By applying principles from athletic recovery and personalized data tracking, clinicians can moderate their performance intensity, enhance their recovery even in short breaks, and prevent long-term burnout. This approach allows emergency physicians to maintain endurance and clarity, improving patient care and team dynamics. ⏩ Things You Can Do on Your Next Shift Measure and Reflect: Start tracking your vital health metrics like heart rate with wearable sensors. Reflect on how daily activities impact these measurements to identify stress patterns.Implement Quick Recovery Techniques: Use short, actionable exercises such as deep breathing or the de-stress breath method between patient encounters to moderate stress levels.Invest in Self-Care: Dedicate brief time slots for essential self-care activities like hydration or quick reflection journaling, aiming to enhance mental resilience throughout your shift.Utilize Coaching Tools: Engage with personalized coaching apps or resources that offer science-backed recovery strategies tailored to your personal and professional needs. 👀 Where to Learn More Intrigued by the possibilities this partnership offers? You can explore more by visiting Arena Labs’ website here. Also, check out the comprehensive coaching program available, designed specifically for healthcare providers looking to enhance their well-being and performance. 🚨 Clinical Bottom Line In an era where burnout is pervasive, our collaboration with Arena Labs offers a beacon of hope for healthcare workers. By leveraging cutting-edge data insights and practical coaching, this partnership aims to redefine healthcare wellness, fostering a sustainable, resilient workforce that’s equipped to navigate the pressures of modern medicine. Join us in this journey towards enhanced well-being and workforce empowerment, ensuring that those who care for us are also cared for. Meet the Authors Mark Ramzy, DO Co-Editor-in-Chief RWJBH / Rutgers Health, Newark NJ Allyn Abadie Principal Scientist Arena Labs REBEL MIND – Growth vs Fixed Mindset in Medicine Mindset shapes everything we do in medicine—from how we teach and learn to ... Human Behavior Read More REBEL MIND – How to Sleep When the World Says You Can’t Today we are exploring the imperative topic of rest and why it’s not ... Human Behavior Read More REBEL MIND: Applying Performance Science In and Out of the Emergency Department In this episode, we're excited to continue collaboration with Arena L

🧭 REBEL Rundown 📌 Key Points The 4 Steps of an ED Consult:👋 Introduce yourself and your role🎯 Lead with the outcome (the ask)🧾 Give a focused case summary (why it’s theirs + what you’ve done)🔁 Close the loop (timeline, next steps, contingencies) Click here for Direct Download of the Podcast. 📝 Introduction Today we’re tackling one of the most important (and most under-taught) skills in emergency medicine: how to call a consult in the ED and what to do when a consultant pushes back.To call a consult in the ED, start with a brief introduction, lead with the outcome you need (“the ask”), give a focused decision-relevant summary, and close the loop with timeline and next steps. If the consultant resists, clarify the “why,” restate the ask, offer alternatives, and escalate when patient safety or disposition is at risk.After two decades in emergency medicine and countless consult calls, here’s a simple framework—plus copy/paste scripts—to make your consults faster, clearer, and easier to say “yes” to. 🤔 Why Consult Skills Matter in Emergency Medicine Consults aren’t a formality—they’re a patient-care intervention. Strong consult communication:Reduces delays in time-sensitive careImproves ED throughput and dispositionDecreases conflict and miscommunicationClarifies ownership and next stepsProtects the patient (and the team) when plans are unclear 🪜 The 4-Step ED Consult Framework (Introduction → Ask → Summary → Close the Loop) Most consult friction comes from one of two problems: unclear expectations or excessive noise. This four-step structure solves both.1) Introduce yourself and your roleA simple intro sets a professional tone and removes ambiguity.Script: “Hey, this is Swami, one of the ED attendings. I’m calling for an ortho consult.” 2) Lead with the outcome (the ask)Don’t bury the lede. The consultant wants to know what you need—immediately.Script: “I’m calling about a patient with a suspected septic knee. I need you to evaluate for operative management.” 3) Give a focused, decision-relevant summaryYour summary should answer:Why this is your service’s problemWhat’s already been doneWhat I’m worried about / what decision is needed nowScript: “43-year-old man with no major PMH, 3 days of knee pain and swelling. XR negative. Febrile. Aspiration yielded purulent fluid—cultures sent. We started antibiotics after the tap. He’s hemodynamically stable.” High-yield pearl: Add quick “stability anchors” when relevant:“Airway stable, pain controlled.”“Neurovascularly intact.”“No signs of compartment syndrome.”“No hypotension or escalating oxygen requirement.” 4) Close the loop (timeline + next steps)This prevents the consult from floating in limbo and protects patient flow.Script: “When do you expect to see the patient, and do you want anything done before you arrive—NPO, repeat labs, additional imaging?” 📝 ED Consult Script General ED Consult Script “Hi, this is Dr. ___ in the ED. I’m calling for a ___ consult. The reason is ___. Briefly: ___ year-old with ___. We’ve done ___ and started ___. I’m concerned about ___. Can you see them today, and what’s your preferred next step?” Septic joint / Ortho Example “Hi, this is Swami in the ED. I need an ortho consult for suspected septic arthritis. 43-year-old with 3 days of atraumatic knee swelling and fever. XR negative. Tap produced purulent fluid—cultures sent. Antibiotics started after aspiration. Can you evaluate for operative management, and when can you see the patient?” Neurology example (time-sensitive) “Hi, this is Dr. ___ in the ED. I need neurology for suspected acute stroke. Last known well ___. NIHSS ___. CT/CTA completed (or pending). I’m calling to discuss candidacy for thrombolysis/thrombectomy and next steps. When can you evaluate and what additional workup do you want now?” ⛓️‍💥 Common ED Consult Mistakes (and Fixes) Mistake: Long story before the askFix: Lead with the outcome in the first sentenceMistake: Unfiltered data dumpFix: Provide only decision-relevant detailsMistake: No timelineFix: Ask explicitly when they’ll see the patient and what they need firstMistake: Implicit “ownership”Fix: Clarify who is admitting, who is following, and what happens if the patient worsens ✋ What to Do When a Consultant Pushes Back Even a perfect consult can meet resistance. Your job is to stay calm, keep it professional, and protect the patient.1) Ask “why?”Don’t argue first—diagnose the refusal.Script: &#x201

🧭 REBEL Rundown 📌 Key Points 💨 HFNC met criteria for non-inferiority to BPAP for preventing intubation or death within 7 days in four of the five ARF subgroups.🧪 Bayesian dynamic borrowing increased power across subgroups but created variable certainty, especially in smaller groups such as COPD.🫁 The immunocompromised hypoxemia subgroup did not meet non-inferiority, leading to early trial stopping for futility.️ Rescue BPAP use, subgroup-specific exclusion criteria, and non-standardized BPAP delivery are important contextual factors that influence how subgroup results should be interpreted. Click here for Direct Download of the Podcast. 📝 Introduction Bilevel Positive Airway Pressure (BPAP) has long been a foundational modality in the management of acute respiratory failure (ARF), particularly in COPD exacerbations and cardiogenic pulmonary edema, where it can rapidly reduce work of breathing and improve gas exchange. It remains a core tool in our respiratory support arsenal.High-flow nasal cannula (HFNC), however, has expanded what we can offer patients by delivering many of the same physiologic benefits through a far more comfortable interface. With high flows, modest PEEP, and effective dead-space washout, HFNC can improve oxygenation and decrease work of breathing while preserving the ability to talk, cough, eat, and interact with staff and family. This combination of physiologic support and tolerability makes HFNC especially attractive in patients where comfort, anxiety, or cardiovascular stability are key considerations, and in settings where prolonged noninvasive support may be needed. Rather than competing with BPAP, HFNC broadens our options in ARF and allows us to better match the modality to the patient and their underlying disease process.The RENOVATE trial set out to answer a high-impact question across five distinct etiologic groups: Is HFNC non-inferior to BPAP (NIV) for preventing intubation or death in acute respiratory failure? 🧾 Paper Azoulay É, et al. High-Flow Nasal Oxygen vs Noninvasive Ventilation in Patients With Acute Respiratory Failure: The RENOVATE Randomized Clinical Trial. JAMA. 2025 PMID: 39657981 🔙Previously Covered On REBEL: HFNC: Part 1 – How It WorksHFNC: Part 2 – Adult and Pediatric IndicationsFLORALI and AVOID TrialFLORALI-2: NIV vs HFNC as Pre-Oxygenation Prior to IntubationThe Pre-AeRATE Trial – HFNC vs NC for RSI ️ What They Did CLINICAL QUESTION Is HFNC non-inferior to BPAP for rate of endotracheal intubation or death at 7 days in patients with acute respiratory failure due to a variety of causes? STUDY DESIGN Multicenter, randomized non-inferiority trial33 Brazilian hospitalsNov 2019 – Nov 2023Adaptive Bayesian hierarchical modeling with dynamic borrowingOpen label, outcome adjudicators blindedPatients were classified into 5 subgroups SUBGROUPS 1. Non-immunocompromised hypoxemiaSpO₂ < 90% on room air orPaO₂ < 60 mm Hg on room air plusIncreased respiratory effort (accessory muscle use, paradoxical breathing, thoracoabdominal asynchrony) orRespiratory rate > 25 breaths/min2. Immunocompromised hypoxemiaDefined as:Use of immunosuppressive drugs for >3 monthsOR high-dose steroids >0.5 mg/kg/dayOR solid organ transplantOR solid tumors or hematologic malignancies (past 5 years)OR HIV with AIDS / primary immunodeficiency3. COPD exacerbation with acidosisHigh clinical suspicion of COPD as primary diagnosisRR >25 with accessory muscle use, paradoxical breathing, and/or thoracoabdominal asynchronyABG: pH <7.35 AND PaCO₂ >454. Acute cardiogenic pulmonary edema (ACPE)Sudden onset dyspnea and rales± S3 heart soundNo evidence of aspiration, infection, or pulmonary fibrosisCXR consistent with pulmonary edema5. Hypoxemic COVID-19 (added June 2023)Added due to deviations between expected and observed outcome proportionsAny patient across the other 4 groups with PCR-confirmed SARS-CoV-2 infection in any of the above groups POPULATION Inclusion Criteria:≥18 yrs with ARF* in one of 5 pre-defined subgroups excluding COPD was defined by the following:Hypoxemia with SpO₂ <90 or PaO₂ <60Accessory muscle use, paradoxical breathing, and/or thoracoabdominal asynchronyRR >25 BPMExclusion Criteria:Need for emergency intubationProlonged apneic episodesCardiorespiratory arrestGCS <12HR <50 with decreased consciousnessABG pH <7.15Severe agitation requiring heavy sedationHemodynamic instability (MAP <65, SBP <90 despite fluids or requiring high-dose pressors)Contraindications to BPAP (facial trauma, recent esophageal surgery, copious secretions, vomiting, aspiration risk)Pneumothorax or large pleural effusionSevere arrhythmiaThoracic trauma as primary ARF causeAsthma attackCardiogenic shockACS requiring urgent cathARF within 72h post-extubationPost-surgical ARF within 72hHypercapnic ARF due to neuro

🧭 REBEL Rundown 🔑Key Points 🛌 Rest isn’t a luxury; it’s a necessity and differs significantly from sleep in terms of mental and physical recovery needs.🧠 Uncovering the seven types of rest can highlight diverse needs: physical, mental, sensory, creative, emotional, social, and spiritual.🏃‍️ Rest from high-stress environments such as the ED is crucial for reducing exhaustion, enhancing decision-making, and maintaining empathy.🔄 The necessity for intentional rest: tailor your rest strategies to meet personal recharge needs effectively.🧐 Rest should be deserved, not earned—it’s a vital component of overall health and wellness, on par with nutrition and hydration. Click here for Direct Download of the Podcast. 👀Previously Covered and Related Content: REBEL Core Cast: Sleep HygieneRebellion in EM: Care For Yourself – Sleep HygieneFirst10EM: Some Evidence For Working Night ShiftsREBEL MIND: Dunning Kruger Effect 📝 Introduction Welcome to this episode of REBEL MIND, where MIND stands for Mastering Internal Negativity during Difficulty. Here we sharpen the person behind the practitioner by focusing on things that improve our performance, optimizing team dynamics and the human behavior that embodies the hidden curriculum of medicine. Today we are exploring the imperative topic of rest and why it’s not just about sleeping. The first of a two part series, hosted by Dr. Mark Ramzy with guests Dr. Maureen Aiad and Dr. Amil Badoolah, our discussion sheds light on the multifaceted nature of rest, especially in the demanding field of emergency medicine. If you’re a clinician striving to perform at your best under pressure, this episode offers valuable insights into achieving the rest you deserve. Cognitive Question How do healthcare professionals in high-stress environments distinguish between rest and sleep, and how can they effectively incorporate various types of rest into their routines to manage stress and improve performance? 💤How is Rest Different From Sleep? Sleep is biological. It’s essential—but it’s only one form of recovery.Rest, on the other hand, is intentional, multifaceted, and active. You can sleep for 8 hours and still feel depleted—because what you needed wasn’t sleep, it was rest—in a different dimension. 🏥How This Applies to the Emergency Department or ICU? In the fast-paced, high-pressure world of the ED or ICU, medical professionals often overlook the importance of rest, perceiving it as unproductive. Yet, rest is crucial for maintaining cognitive function and emotional resilience. The unique concept of rest outlined in the ‘seven types of rest’ can be particularly beneficial. Understanding and implementing these can help practitioners handle the rigors of patient care and decision-making more effectively. 7️⃣The Seven Types of Rest 1️⃣Physical Rest: Passive (like sleep) and active (like stretching, massage, gentle movement).2️⃣Mental Rest: Reducing decision fatigue. Tools like brain dumping, meditation, or taking real breaks during work.3️⃣Sensory Rest: This involves reducing the input from your senses, such as limiting screen time, turning off the lights, or enjoying quiet time.4️⃣Creative Rest: Reconnecting with awe. Nature, art, music—things that refill your inspiration tank5️⃣Emotional Rest: Being around people you don’t have to perform for. Saying “I’m not okay.” spaces and people where you can be your authentic self and be at peace6️⃣Social Rest: Taking space from draining interactions; spending time with life-giving people. 7️⃣Spiritual Rest: Connection to a greater purpose—faith, community, reflection, meditation ⏩Immediate Action Steps for Your Next Shift **Identify Your Rest Needs**: Reflect on what kind of fatigue you’re experiencing and tailor rest activities accordingly, whether it’s sensory detox or emotional unwinding.**Practice Sensory Rest**: Take brief moments to close your eyes, or step outside for fresh air to manage overstimulation during shifts.**Plan Intentional Breaks**: Schedule specific times for rest that focus on particular dimensions you identify as lacking.**Engage in Active Rest**: Incorporate activities like stretching or meditation during your breaks to enhance mental clarity and reduce physical exhaustion.**Connect with Supportive Colleagues**: Seek interactions with peers who offer emotional and social support, promoting a healthy work-life balance. 🛌🏽The Many Aspects of What Makes Up Rest Rest is multifaceted – it comes in more than one formRest is productive – it improves performance, decision-making, empathyRest is intentional – it re

🧭 REBEL Rundown 🗝️ Key Points 💉 Hydrocortisone Saves Lives:The 2023 Cape Cod Trial (NEJM) showed a clear mortality benefit and reduced need for intubation in severe CAP patients treated with hydrocortisone.📊 Guidelines Are Catching Up:The SCCM (2024) and ERS now recommend steroids for severe CAP, while ATS/IDSA updates are still pending.🔥 Redefining “Severe”:Patients requiring high FiO₂ (>50%), noninvasive or mechanical ventilation, or PSI >130 meet criteria for steroid therapy — even outside the ICU.🍬 Main Risk = Hyperglycemia:Elevated glucose was the most consistent adverse effect, but rates of GI bleed and secondary infection were not increased.🧭 Early, Targeted Use Matters:Start hydrocortisone within 24 hours of identifying severity — especially in patients with high CRP (>150) or strong inflammatory response. Click here for Direct Download of the Podcast. 📝 Introduction Corticosteroids have long sparked debate in the treatment of bacterial pneumonia — once viewed with skepticism, now increasingly supported by high-quality evidence. In this episode, Dr. Alex Chapa joins the REBEL Core Cast team to explore how the 2023 Cape Cod Trial (NEJM) reshaped practice and guideline recommendations for severe community-acquired pneumonia (CAP). 📖 Historical Context & Long-Standing Skepticism For decades, the use of steroids in pneumonia was controversial.Early Use: Steroids entered practice in the 1940s and 50s for autoimmune inflammation, but there was immediate hesitation regarding secondary superinfections.Mixed Data: From the 1980s to the 2000s, small studies emerged on severe pneumonia and ARDS, but the data was inconsistent. Different trials used varying definitions of “severe” pneumonia and different C-reactive protein (CRP) cutoffs, making the data “spread” and easy to “cherry pick” to support or deny a benefit.Past Guidelines: This uncertainty was reflected in official guidelines:2007 (ATS/IDSA): The American Thoracic Society and the Infectious Diseases Society of America did not address the topic due to insufficient data.2019 (ATS/IDSA): Pre-COVID, the guidelines recommended against using corticosteroids in severe CAP. They acknowledged no benefit for non-severe pneumonia, but the data for severe pneumonia was considered too weak to endorse.Pre-Trial Consensus: Prior to 2023, the consensus was to avoid steroids in non-severe pneumonia, while severe pneumonia remained a “gray area” with no treatment showing a clear mortality difference. 📜 The Landmark Cape Cod Trial (NEJM 2023) The Cape Cod trial, published in the New England Journal of Medicine in 2023, reignited the discussion by providing robust, positive data.Trial Design: Phase 3, multi-center, double-blind, randomized, controlled trial.Intervention: 800 patients randomized to two groups, Hydrocortisone as a continuous infusion (200mg/day) versus a placebo infusion.Taper: On day 4, clinicians would decide whether to continue the infusion or begin a taper based on clinical response.Population: Patients with severe CAP, defined by meeting at least one of the following criteria:Pneumonia Severity Index (PSI) > 130.O2 by FiO2 ratio < 300.Need for mechanical or non-invasive ventilation (with PEEP ≥ 5).Need for high FiO2 (>50%) via non-rebreather or heated high flow.Primary Outcomes: Death for any cause 6.2% (hydrocortisone) vs 11.9% (placebo)Secondary outcomes:Death from any cause at 90 days 9.3% (hydrocortisone) vs 14.7% (placebo)Endotracheal intubation 18% (hydrocortisone) vs 29% (placebo)Hospital-acquired infections 9.8% (hydrocortisone) vs 11.1% (placebo)Gastrointestinal bleeding 2.3% (hydrocortisone) vs 3.3% (placebo)Vasopressor initiation by day 28 15.3% (hydrocortisone) vs 25.0% (placebo)Key Findings: The trial demonstrated superiority for hydrocortisone 📋 Updated Guidelines & Current Practice The Cape Cod trial, along with subsequent meta-analyses, has begun to change official recommendations.Society of Critical Care Medicine (SCCM): In 2024, an SCCM expert panel, reviewing the Cape Cod trial and 18 others, strongly recommended corticosteroids for severe CAP. They concluded that steroids reduce mortality and the need for mechanical ventilation.Meta-Analysis (Smit et al.): A 2024 meta-analysis in Lancet Respiratory confirmed the 30-day mortality benefit.European Respiratory Society (ERS): The ERS has issued a recommendation to use steroids for severe pneumonia but still urges caution regarding side effects.ATS/IDSA: As of the podcast recording, the ATS/IDSA had not yet updated their 2019 guidelines. 🛠️ Practical Application for Clinicians Defining “Severe” CAP: The key is to identify patients who qualify as “severe”. This can be done using:Scoring Tools: The PSI is the best validated tool for mortalit

🧭 REBEL Rundown 📝Introduction Welcome to this special edition of the REBEL Cast, where we unravel key highlights and educational insights from the IncrEMentuM Conference in Spain. This event is a cornerstone for advancing emergency medicine education, drawing esteemed speakers and participants from around the globe. As emergency medicine gains traction in Spain, this conference has become an essential platform for knowledge exchange and professional growth. Today, host Dr. Mark Ramzy shines a spotlight on two phenomenal educators: Drs. Sara Crager and Ryan Ernst who shared their expertise and experiences at this transformative gathering last spring. Click here for Direct Download of the Podcast. 🤔What's IncrEMentuM? A new conference and a pivotal gathering for emergency medicine professionals worldwide, has become an essential platform for education, collaboration, and advocacy, especially in light of emergency medicine’s recent recognition as a specialty in Spain. The conference is praised for its outstanding production quality, engaging speakers, and its capacity to foster a global community of emergency care professionals. ️What's an Essential Question? Essential questions are open-ended, thought-provoking, and intellectually engaging inquiries that inspire deeper exploration into topics. In the context of medical education, they challenge practitioners to think critically and reflect on their practice deeply. By focusing on essential questions, medical educators aim to inculcate a culture of continuous learning and curiosity, ensuring that medical professionals stay adaptable and insightful in their approach to patient care. 🎮Rapid Sequence (no not the intubating style...)  The Rapid Sequence game is an innovative tool that Sara and Ryan designed to enhance the learning experience for emergency medicine clinicians. It mimics real-life scenarios requiring rapid decision-making in high-pressure situations, such as those faced in emergency medical settings. This clinical case-based game aims to improve cognitive and procedural skills, allowing participants to hone their ability to respond effectively under pressure, thereby enhancing their real-world clinical performance.You can try it out for free on their website here!Their work was featured in the September 2025 edition of Annals of Emergency Medicine as a 2025 ACEP Abstract 🌳The Arboretum Teaching Collective An arboretum is a space that cultivates a wide variety of diverse, unique, and symbiotic growth. Arboretum provides a creative space to decrease barriers, open opportunities, and support the development of extraordinary teachers. The Arboretum Teaching Collective is a non-profit organization dedicated to supporting emergency medicine education in countries where it is a new or evolving specialty.  Their aim to facilitate the development of expert teachers by reducing barriers, providing opportunities, and curating talent.  Their goal is to create a community of educators around the globe who share a vision of bringing excellent, innovative emergency medicine teaching to where it is most needed.  Their approach is driven by curiosity, humility, and sustainability.If you want to learn more and get involved, check out the Arboretum Teaching Collective Website Here ️ See you in Spain! The upcoming conference aims to gather world-class educators once more and promises an enriching experience for all attendees. Drs. Sara Crager and Ryan Ernst, along with many others, will be there at the event. For more information on the IncrEMentuM Conference and to register, visit their website! See you there! Sara Crager, MD Associate Professor, Critical Care and Emergency Medicine UCLA, Los Angeles, CA Ryan Ernst, MD Assistant Professor of Emergency Medicine, Section Chief of Global EM University of Utah, Salt Lake City, UT Mark Ramzy, DO Co-Editor-in-Chief Rutgers Health / RWJBH, Newark, NJ 🔎 Your Deep-Dive Starts Here REBEL CAST – IncrEMentuM26 Speaker Spotlight : Drs. Sara Crager and Ryan Ernst Host Dr. Mark Ramzy shines a spotlight on two phenomenal ... Resuscitation Read More REBEL CAST – IncrEMentuM26 Speaker Spotlight : Drs. Tarlan Hedayati, Jess Mason and Simon Carley Host Dr. Mark Ramzy shines a spotlight on three distinguished ... Resuscitation Read More REBEL CAST – IncrEMentuM26 Speaker Spotlight : George Willis and Mark Ramzy 🧭 REBEL Rundown 📝Introduction In this exciting episode of REBEL ... Endocrine, Metabolic, Fluid, and Electrolytes Read More Incrementum Conference 2026: Revolutionizing Emergency Medicine in Spain In this special episode of Rebel Cast, we spotlight the ... Read More The post REBEL CAST – IncrEMentuM26 Speaker Spotlight : Drs. Sara Crager and Ryan Ernst appeared first on REBEL EM - Emergency Medicine Blog.

🧭 REBEL Rundown 📌 Key Points 💪 Building Resilience: Rebel MIND, in partnership with Arena Labs, introduces a science-based performance coaching platform specifically tailored for healthcare professionals, focusing on stress management and burnout prevention.🤝 Personal Insights: Jackie Penn shares her journey from exercise science to digital coaching, highlighting the importance of tailored coaching in high-pressure environments like healthcare.🎯 Clinician-Centric Approach: Understanding unique challenges faced by ER doctors, the program provides practical tools for stress and transition management, improving both professional and personal life balance.💻 Revolutionary Wearables: Utilizing wearables, the program offers objective feedback on recovery and health metrics, allowing personalization of strategies to enhance clinician well-being. Click here for Direct Download of the Podcast. 📝 Introduction Welcome back to REBEL MIND, where MIND stands for Mastering Internal Negativity during Difficulty. Here we sharpen the person behind the practitioner by focusing on things that improve our performance, optimizing team dynamics and the human behavior that embodies the hidden curriculum of medicine. In this episode, we’re excited to continue collaboration with Arena Labs, where host Dr. Marco Propersi interviews Jackie Pen, Heading of Performance Coaching at Arena Labs. Arena Labs is helping us measure healthcare performance through innovative programs designed to combat burnout and enhance personal wellness using data-driven strategies.  🔙Previously Covered on REBEL MIND: Performance Under Pressure – What Medicine Can Learn from Elite Teams 🤔Cognitive Question How do specific performance coaching strategies and tools assist healthcare professionals, particularly those in emergency medicine, in managing stress and preventing burnout effectively? 💭 Why This is Important Burnout among healthcare workers is a growing concern, especially in such high-pressure environments as emergency and intensive care units. The collaboration with Arena Labs brings forth a vital focus on using data and coaching to build resilience among medical professionals. 🏥How This Applies to the Emergency Department or ICU? In the chaotic and high-stakes environment of the ED/ICU, healthcare professionals are often required to make split-second decisions under pressure while managing emotional stress. This necessitates not just clinical acumen but also strong emotional resilience and stress management skills. Performance coaching provides the tools and frameworks to enhance these skills, offering strategies like the de-stress breath and transition protocols to help clinicians navigate between high-pressure situations efficiently. These tools are designed to not only improve their professional performance but also ensure they are emotionally present for their personal lives, ensuring a healthier work-life balance. ⏩ Things You Can Do on Your Next Shift Practice the De-stress Breath: Before moving from one critical case to another, take a moment to take two inhales through the nose followed by an extended exhale, helping to reset your nervous system by activating your parasympathetic nervous system.Implement a Transition Protocol: Choose a point in your journey home to mentally switch from clinician to family member, helping you to be more present outside of work.Optimize Your Nutrition and Rest: Even small changes during your shift, like meals that promote easy digestion or quick physical activities, can make a significant difference in your energy levels.Engage with Wearables: If possible, use wearables to monitor your physiological responses, helping tailor personalized strategies for your shifts 👀 Where to Learn More Intrigued by the possibilities this partnership offers? You can explore more by visiting Arena Labs’ website here. Also, check out the comprehensive coaching program available, designed specifically for healthcare providers looking to enhance their well-being and performance. 🚨 Clinical Bottom Line In an era where burnout is pervasive, our collaboration with Arena Labs offers a beacon of hope for healthcare workers. By leveraging cutting-edge data insights and practical coaching, this partnership aims to redefine healthcare wellness, fostering a sustainable, resilient workforce that’s equipped to navigate the pressures of modern medicine. Join us in this journey towards enhanced well-being and workforce empowerment, ensuring that those who care for us are also cared for. Meet the Authors Marco Propersi Co-Editor-in-Chief Vassar Brothers Medical Center, Poughkeepsie, NY Jackie Pen Head of Performance Coaching Arena Labs The post REBEL MIND: The Power of Performance Coaching in Medicine appeared first on REBEL EM - Emergency Medicine Blog.

🧭 REBEL Rundown 📌 Key Points 🎯Partnership Focus: New collaboration with Arena Labs aimed at enhancing healthcare worker wellness.🏃🏽‍️‍➡️Personalized Coaching: Tools and coaching programs designed for stress management and performance improvement.📊Data-Driven Insights: Utilizing wearable sensor data to tackle burnout effectively.🌄Broad Impact: Offers a unique opportunity to contribute to large-scale healthcare improvements. Click here for Direct Download of the Podcast. 📝 Introduction Welcome back to REBEL MIND, where MIND stands for Mastering Internal Negativity during Difficulty. Here we sharpen the person behind the practitioner by focusing on things that improve our performance, optimizing team dynamics and the human behavior that embodies the hidden curriculum of medicine. In this episode, hosted by Drs. Mark Ramzy and Marco Propersi, we’re excited to introduce a collaboration with Arena Labs. Arena Labs is helping us measure healthcare performance through innovative programs designed to combat burnout and enhance personal wellness using data-driven strategies.  Cognitive Question What would it look like in emergency medicine and critical care to be set up with the same tools as elite teams and professional athletes when it comes to measuring performance and recovery? How would our patients benefit? 💭 Why This is Important Burnout among healthcare workers is a growing concern, especially in such high-pressure environments as emergency and intensive care units. The collaboration with Arena Labs brings forth a vital focus on using data and coaching to build resilience among medical professionals. 🌟Be Brilliant at the Basics Ask yourself — “What is it on your time off that gives you a deep sense of fulfillment?”On your time off are you doing things that fill your bucket and add to your recovery? What is Allostasis and Allostatic Load Allostasis: Our body’s ability to adapt over time to stress. It’s relevant to the phase you are in during this particular season in your life. Ex. You are a first year medical student freaking out about your very first exam. Over time as you do more exams, they are still stressful, but by now you have developed modified study habits to succeed and get used to the frequent examsIn the context of emergency medicine, you may be nervous or stressed about your first shift at a new hospital but overtime you learn the staff, the location of equipment, the acuity of that particular site, the patient population so over time you get used to the stress of a shift at that new hospitalAllostatic Load: The wear and tear on the body from chronic stress due to maladaptation or poor recovery methods.This refers to the cumulative burden of chronic stress and life events. It involves the interaction of different physiological systems at varying degrees of activity.Ex. You are an emergency medicine physician at a very busy, high acuity center and have never prioritized taking care of yourself on/during a shift. As a result, external factors add to not being able to fully recover when you get home or are off shift (ie. Admin work, teaching obligations, family/friends) and so you never fully recover before you have to go back on shift to the same stressors you just exposed yourself to. So the cycle continuesFigure 1: Long term effects of Chronic Stress (Source: Andrew Hogue from NeuroFit) 🏥How This Applies to the Emergency Department or ICU? Healthcare workers in emergency departments (ED) and intensive care units (ICU) are often under enormous stress due to the nature of their work. Arena Labs’ program offers tailored solutions, helping ED and ICU staff manage their unique challenges through effective recovery techniques and performance tools. This approach caters specifically to the demanding schedules and the unpredictability inherent in these environments. 👀 Where to Learn More Intrigued by the possibilities this partnership offers? You can explore more by visiting Arena Labs’ website here. Also, check out the comprehensive coaching program available, designed specifically for healthcare providers looking to enhance their well-being and performance. 🚨 Clinical Bottom Line In an era where burnout is pervasive, our collaboration with Arena Labs offers a beacon of hope for healthcare workers. By leveraging cutting-edge data insights and practical coaching, this partnership aims to redefine healthcare wellness, fostering a sustainable, resilient workforce that’s equipped to navigate the pressures of modern medicine. Join us in this journey towards enhanced well-being and workforce empowerment, ensuring that those who care for us are also cared for. 📚References Guidi J, et al.Allostatic Load and Its Impact on Health: A Systematic Review. Psychother Psychosom. 2021; Epub 2020 Aug 14.

🧭 REBEL Rundown 🗝️ Key Points 💨 NIV = Support without a tube: CPAP, BiPAP, and HFNC improve oxygenation and reduce the work of breathing.🫁 CPAP = Continuous pressure: Best for hypoxemic patients (e.g., pulmonary edema, OSA).️ BiPAP = Two pressures (IPAP/EPAP): Great for hypercapnic failure (e.g., COPD, obesity hypoventilation).🌬️ HFNC = Heated, humidified high flow: Reduces effort, improves comfort, and enhances oxygen delivery.🩺 Supportive, not definitive: NIV stabilizes patients while the underlying cause is treated. Click here for Direct Download of the Podcast. 📝 Introduction Non-invasive ventilation (NIV) refers to respiratory support provided without endotracheal intubation. The most common modalities include continuous positive airway pressure (CPAP), bilevel positive airway pressure (BiPAP), and high-flow nasal cannula (HFNC). These therapies aim to improve oxygenation, reduce the work of breathing, and potentially prevent invasive mechanical ventilation. 💨 CPAP and BiPAP CPAP delivers a single, continuous pressure during inspiration and expiration. This pressure (commonly 5–10 cm H₂O) helps recruit atelectatic alveoli, reduce shunt, and improve oxygenation. It is commonly used for conditions like pulmonary edema, obstructive sleep apnea, or mild hypoxemia without significant ventilatory failure.BiPAP alternates between two pressures:Inspiratory positive airway pressure (IPAP), augments tidal volume and unloads inspiratory muscles.Expiratory positive airway pressure (EPAP), maintains alveolar recruitment and improves oxygenation.The differential between IPAP and EPAP is critical for reducing hypercapnia in patients with COPD exacerbations or acute hypercapnic respiratory failure.IndicationsCPAP: hypoxemia without major ventilatory failure (e.g., cardiogenic pulmonary edema, atelectasis, OSA).BiPAP: hypercapnia with increased work of breathing (e.g., COPD exacerbation, neuromuscular weakness, obesity hypoventilation).A helpful way to conceptualize CPAP and BiPAP is through the hairdryer analogy. Imagine placing a hairdryer in your mouth: 🩺 Clinical Considerations Masks can be uncomfortable, impair secretion clearance, and limit oral intake.Some patients require sedation to tolerate NIV, but this carries risks in patients with unprotected airways.NIV is thus a high-stakes intervention requiring close monitoring.Common starting dose to understand titration, but start at the level appropriate for your patient:  IPAP 10 cm H₂O / EPAP 5 cm H₂O (“10/5”) and are titrated:Increase IPAP to improve tidal volume and CO₂ clearance.Increase EPAP to recruit alveoli and improve oxygenation.Both may be raised simultaneously if the patient is both hypoxemic and hypercapnic. 🚀 High-Flow Nasal Cannula (HFNC) H: Heated & humidified – improves mucociliary clearance, prevents airway drying, and enhances tolerance. I: Inspiratory flow – high flow meets or exceeds patient demand, reducing respiratory rate and effort.F: Functional residual capacity – modest generation of positive end-expiratory pressure (PEEP), promoting alveolar recruitment.L: Lighter – generally more comfortable and less restrictive than mask-based NIV.O: Oxygen dilution – minimizes entrainment of room air, delivering higher and more predictable FiO₂.W: Washout – flushes anatomical dead space, reducing CO₂ rebreathing.HFNC delivers heated, humidified oxygen at high flow rates (30–60 L/min) through wide-bore nasal prongs. A mnemonic, H-I-F-L-O-W, helps summarize its mechanisms:Indications: Traditionally used for acute hypoxemic respiratory failure (e.g., pneumonia), HFNC is increasingly studied for hypercapnic failure as well, with trials suggesting non-inferiority to BiPAP in select populations. Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO) 👤 Show Notes Syed Moosi Raza, MD PGY 3 Internal Medicine Resident Cape Fear Valley Internal Medicine Residency Program Fayetteville NC Aspiring Pulmonary Critical Care Fellow 🔎 Your Deep-Dive Starts Here REBEL Core Cast 137.0: A Simple Approach to Sinus Tachycardia Sinus tachycardia is the most prevalent cardiac dysrhythmia in critically ... Cardiovascular Read More REBEL Core Cast 136.0: A Simple Approach to the Tachypneic Patient In this episode, we focus on the bedside evaluation of ... Thoracic and Respiratory Read More REBEL Core Cast 1.0 – The Intro REBEL EM-ers: Salim, Jenny and I would like to announce ... Read More The post REBEL Core Cast 148.0–Demystifying Non-Invasive Ventilation & HiFlow appeared first on REBEL EM - Emergency Medicine Blog.

🧭 REBEL Rundown 📌 Key Points 💀 Mortality: No statistically significant difference in 28-day mortality between ketamine vs etomidate for intubation in critically ill patients, though there was a ~1% absolute difference favoring ketamine. 📉🫀⚠️ Hemodynamics: Ketamine induction was associated with more cardiovascular collapse, mainly driven by new/increased vasopressor use (dose escalation or addition of a vasoactive agent). 💉⬆️ Click here for Direct Download of the Podcast. 📝 Introduction Etomidate or ketamine? The debate over the ideal agent for emergency rapid sequence intubation (RSI) has raged for years with no clear winner. Etomidate has been touted in the past for its rapid onset and minimal intrinsic effects on hemodynamics. However, the drug is well known as a transient adrenal suppressant though the impact of this suppression isn’t clear. Ketamine has risen in recent years as an alternative, due to its perceived hemodynamic stability, analgesic properties and absence of adrenal suppression. Additionally, recent data points towards improved mortality when ketamine was selected over etomidate (Kotani 2023). High quality randomized controlled trials are needed to further elucidate which agent should be selected in critically ill patients. 🧾 Paper Casey JD et al. Ketamine or etomidate for tracheal intubation of critically ill adults. NEJM 2025. PMID: 41369227 🔙Previously Covered On REBEL REBEL EM: The EvK Trial: Ketamine vs Etomidate for Rapid Sequence IntubationREBEL EM: From Debate to Data: Emerging Insights into RSI Induction with Ketamine vs Etomidate ️ What They Did CLINICAL QUESTION In critically ill adults undergoing tracheal intubation, does the use of ketamine instead of etomidate result in improved 28 day mortality? STUDY DESIGN Multicenter, randomized, open-label trial in both emergency departments and ICUs. POPULATION Inclusion Criteria:Critically ill patients > 18 years of age undergoing tracheal intubation with the use of an induction agentExclusion Criteria:Known pregnancyPrisonersPrimary diagnosis of traumaNeed for immediate intubation precluding randomizationClinicians determined that the use of ketamine or etomidate was either necessary or contraindicated INTERVENTION & COMPARATOR Ketamine Arm:Ketamine administered based on a provided nomogram: full dose (2.0 mg/kg), intermediate dose (1.5 mg/kg) or reduced dose (1.0 mg/kg)Etomidate Arm:Etomidate administered based on a provided nomogram: full dose (0.3 mg/kg), intermediate dose (0.25 mg/kg) or reduced dose (0.2 mg/kg) OUTCOMES Primary: In-hospital death from any cause by day 28.Secondary:Cardiovascular collapse during intubation defined as SBP < 65 mm Hg, receipt of new or increased dose of vasopressors or cardiac arrest.Exploratory Procedural:Lowest systolic blood pressureLowest systolic blood pressure below 80 mmHgHighest systolic blood pressure above 180 mmHgLowest oxygen saturationLowest oxygen saturation below 80%Successful first attempt intubationTime from induction to intubationExploratory Clinical:Number of ventilator free daysVasopressor-free daysICU free days Safety: Systolic blood pressure at 24 hours after enrollmentOngoing receipt of vasopressors at 24 hours 📈 Results: 2365 patients were randomizedKetamine: 1176Etomidate: 1189> 99% of patients received the drug they were randomized to receiveNMBA: 69% of patients in both groups received rocuronium~ 95% of patients had video laryngoscopy for the primary intubation attempt 💥 Critical Results 💪 Strengths Multicenter ED + ICU cohort of critically ill patients → improves external validityStrong randomization → balanced baseline characteristicsRight population for the question → appropriately focused on a sick cohort where induction choice matters mostHigh protocol adherence → most patients received the agent they were randomized toExcellent follow-up → minimal loss to follow-up / outcome capture ⚠️ Limitations No blinding → potential performance/resuscitation biasTrauma excluded → limits applicability to peri-intubation trauma careCase-mix skewed toward septic shock → may reduce generalizability to other shock etiologiesPower assumptions → designed to detect a 5% mortality difference (possibly overly ambitious)Equipoise-only enrollment → excluded patients with clear indication/contraindication → selection bias + reduced real-world applicabilityComposite secondary outcome with non-equivalent endpoints (e.g., cardiac arrest vs vasopressor titration)Ketamine dosing by actual body weight (vs ideal) → may have increased dose/exposure in some patients 🗣️ Discussion The increase in cardiovascular collapse seen with ketamine was driven by the “new or increased vasopressor use” piece of the composite outc

🧭 REBEL Rundown 📌 Key Points 🧠 We don’t know what we don’t know: Low experience can inflate confidence; true expertise usually brings humble certainty.🏥 ED relevance is universal: From central lines to transvenous pacing, over- or under-confidence shows up at every level—intern to seasoned attending.🧩 Metacognition matters: Accurate self-assessment is a clinical skill; reflection + feedback loops keep us calibrated.🛠️ Practice beats bravado: Skill decay is real; deliberate practice and HALO (high-acuity, low-occurrence) refreshers protect patients.🤝 Psychological safety ≠ niceties: “Confident humility” enables questions, feedback, and better resuscitation decisions—especially under uncertainty. Click here for Direct Download of the Podcast. 📝 Introduction Welcome to REBEL MIND—Mastering Internal Negativity during Difficulty. In this series, we turn the same critical lens REBEL EM uses for literature inward—into mindset, leadership, and psychological safety—so we can deliver better care outward to patients and teams.In this episode and blog post, hosts Mark Ramzy and Kim Bambach (Assistant Professor of Emergency Medicine, The Ohio State University) explore a deceptively simple question: How accurately can we assess our own performance? The answer hinges on a classic cognitive bias that touches all of us in emergency medicine. 🧾 Paper Kruger J, Dunning D. Unskilled and unaware of it: how difficulties in recognizing one’s own incompetence lead to inflated self-assessments. J Pers Soc Psychol. 1999 Dec;7 PMID: 10626367 Cognitive Question How accurately can we assess our own performance? 💭 What is the Dunning-Kruger Effect? The Dunning–Kruger Effect is a cognitive bias where:Lower-skill individuals tend to overestimate their competence, andHigher-skill individuals often underestimate theirs.Translation for the busy clinician: early on the learning curve, confidence spikes (“Mount Stupid”) because we don’t yet see the complexity. As experience accrues, confidence dips (“Valley of Despair”) with growing awareness, then rises again—grounded in nuance and humility.Key insight: True expertise ≠ louder certainty; it’s often quieter, more curious, and more collaborative. How It Applies to the Emergency Department Procedures (e.g., central lines, TVP): Watching a 5-minute video creates “I got this” energy—until the wire won’t pass, the patient thrashes, or you hit carotid. Competence includes troubleshooting in context.Skill Decay is Inevitable: If you haven’t done a chest tube or a TVP in months, you’re not as sharp as last time. Without deliberate refreshers, you drift below the safe-performance line.Everyone’s a Novice Somewhere: New disease entities, evolving algorithms, new tools (POCUS, decision support) mean even attendings routinely re-enter novice zones.Feedback Blind Spots: Lower performers can both overestimate their skills and resist feedback—while many high performers (particularly women, per discussed literature) undervalue their abilities.Culture is Clinical: The ED demands decisive action amid uncertainty. Psychological safety + confident humility lets teams surface alternative diagnoses, challenge momentum, and correct course fast. ⏩Immediate Action Steps for Your Next Shift Run a 60-second debrief on two casesWhat went well? What would I do differently next time? Write one improvement you’ll test today.Play “What if the opposite were true?”Anchored on “lumbosacral strain”, Ask, What if fever/incontinence appears? How does that change my path?Solicit 360° micro-feedbackAsk a nurse, resident, and peer: “One thing I did well; one thing to improve.” Say “thank you,” not “but.”Schedule a HALO refresher this weekPick one high-acuity, low-occurrence procedure (TVP, cric, thoracotomy). Do a 10-minute mental model + equipment walk-through; book sim time if available.Adopt a pre-procedure pauseIf X goes wrong, I’ll do Y. Name two likely failure modes (e.g., “wire won’t advance,” “delirium/agitation”) and your first corrective step.Language shift on shiftSwap “I’m sure” → “I’m reasonably confident, here’s my plan B.” Invite input: “What am I missing?” Conclusion The Dunning–Kruger Effect isn’t a moral failing; it’s a predictable human pattern that every clinician rides—often multiple times per day in the ED. The antidote is metacognition: routine reflection, explicit debiasing, deliberate practice, and feedback within a psychologically safe culture. 🚨 Clinical Bottom Line Competence is qui

🧭 REBEL Rundown 🗝️ Key Points 💨 Peak vs. Plateau Pressures: PIP reflects total airway resistance and compliance, while Pplat isolates alveolar compliance—elevations in both suggest decreased lung compliance (e.g., ARDS, pulmonary edema, pneumothorax).🧱 PEEP Protects Alveoli: Maintains alveolar recruitment and prevents collapse; typical range 5–8 cmH₂O, but higher levels may benefit moderate–severe ARDS.️ Driving Pressure (ΔP = Pplat − PEEP): Lower ΔP reduces atelectrauma and improves outcomes; optimize by adjusting PEEP thoughtfully.💥 Prevent VILI: Keep Pplat < 30 cmH₂O, use low tidal volumes (6 mL/kg IBW), and monitor for barotrauma, volutrauma, atelectrauma, and biotrauma.📚 Evidence-Based Practice: ARDSNet and subsequent trials confirm that lung-protective ventilation—low Vt, limited pressures, and individualized PEEP—improves survival in ARDS. Click here for Direct Download of the Podcast. 📝 Introduction This episode reviews essential ventilator pressures and how to interpret them during ICU rounds. 🚀 Under Pressure Peak Inspiratory Pressure (PIP)Definition: Total pressure required to deliver a breath.Reflects: Airway resistance + lung/chest wall compliance.Common Causes of ↑ PIP:Mucus pluggingBiting the endotracheal tubeKinked tubing or bronchospasmPlateau Pressure (Pplat)Definition: Alveolar pressure measured after an inspiratory hold.Reflects: Lung compliance (stiffness of lung tissue).When Both PIP & Pplat Are Elevated:→ Indicates poor compliance (e.g., ARDS, pulmonary edema, pneumothorax).Positive End-Expiratory Pressure (PEEP)Definition: Pressure remaining in airways at end-expiration to prevent alveolar collapse.Typical Range: 5–8 cmH₂O but needs to titrated to meet patient requirements Notes:Provides physiologic “glottic” PEEP in intubated patients.Using high PEEP strategy shows mortality benefit only in moderate–severe ARDS in meta-analysis.Driving Pressure (ΔP)Definition: ΔP = Pplat − PEEP.Reflects: Pressure needed to keep alveoli open during the respiratory cycle.Goal: Lower ΔP → less atelectrauma & improved outcomes.Optimize: Increase PEEP to reduce ΔP and alveolar cycling. 📖 Interpreting High PIP/High Pplat ↑ PIP & ↑ PplatInterpretation: ↓ ComplianceCommon Causes: ARDS, pulmonary edema, pleural effusion, pneumothorax↑ PIP & Normal/Low PplatInterpretation: ↑ Airway ResistanceCommon Causes: Mucus plug, bronchospasm, tube obstruction or biting 🤕 Ventilator-Associated Lung Injury (VILI) Barotrauma:Mechanism: Excessive airway pressure damages alveoli.Prevention: Keep Pplat < 30 cmH₂O.Volutrauma:Mechanism: Overdistension from excessive tidal volumes.Prevention: Use low tidal volume ventilation (6 mL/kg ideal body weight).ARDSNet trial: 6 mL/kg → lower mortality compared to 12 mL/kg.Ideal Body Weight: Based on height and sex, not actual weight.Typical patient: Tidal Volume: 6–8 mL/kg IBWARDS: Tidal Volume: 4–6 mL/kg IBWAtelectrauma:Mechanism: Repeated opening/collapse of unstable alveoli.Prevention: Optimize PEEP to keep alveoli open and reduce driving pressure.Biotrauma:Mechanism: Inflammatory cascade (↑ IL-6, TNF-α) from mechanical injury.Effect: Can trigger systemic inflammation & multiorgan dysfunction.Prevention: Minimize all other forms of VILI. Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO) 👤 Show Notes Joel Rios Rodriguez, MD PGY 3 Internal Medicine Resident Cape Fear Valley Internal Medicine Residency Program Fayetteville NC Aspiring Pulmonary Critical Care Fellow 🔎 Your Deep-Dive Starts Here It seems we can't find what you're looking for. The post REBEL Core Cast 147.0–Ventilators Part 5: Key Mechanical Ventilator Pressures & Definitions Made Simple appeared first on REBEL EM - Emergency Medicine Blog.

🧭 REBEL Rundown 🗝️ Key Points ❌ Don’t chase perfect numbers: Adequate and safe is often better than “perfect but harmful.”💨 Oxygenation levers: Start with FiO₂ and PEEP, but remember MAP is the true driver.🫁 Ventilation levers: Adjust RR and TV, tailored to underlying physiology.🚫 Watch your obstructive patients: Sometimes less RR is more. Click here for Direct Download of the Podcast. 📝 Introduction Ventilator management can feel overwhelming—there are so many knobs to turn, numbers to watch, and changes to make. But before adjusting any settings, it’s crucial to understand why the patient is in distress in the first place, because the right strategy depends on the underlying cause. In this episode, we’ll walk through three different cases to see how the approach changes depending on the problem at hand. ️ The 4 Main Ventilator Settings  Tidal Volume (Vt) 🌬️ Amount of air delivered with each breath Typically set based on ideal body weight (6–8 mL/kg for lung protection) Respiratory Rate (RR) ⏱️ Number of breaths delivered per minute Adjusted to control minute ventilation and manage CO₂  FiO₂ (Fraction of Inspired Oxygen) ⛽ Percentage of oxygen delivered Adjusted to maintain adequate oxygenation (goal SpO₂ 92–96%, PaO₂ 55–80 mmHg). PEEP (Positive End-Expiratory Pressure) 🎈 Pressure maintained in the lungs at the end of exhalation to prevent alveolar collapse and improve oxygenation 🧮 Modes of Ventilation AC/VC (Assist Control – Volume Control)How it Works: Delivers a set tidal volume with each breath (whether patient- or machine-triggered).When It’s Used / Pros: Most common initial mode; guarantees minute ventilation; good for patients with variable effort.Limitations / Cons: May cause patient–ventilator dyssynchrony if set volumes don’t match patient’s demand.AC/PC (Assist Control – Pressure Control)How it Works: Delivers a set inspiratory pressure for each breath; tidal volume varies depending on lung compliance/resistance.When It’s Used / Pros: Useful in ARDS (lung-protective strategy), limits peak airway pressures.Limitations / Cons: Tidal volume not guaranteed; must closely monitor volumes and minute ventilation.PRVC (Pressure-Regulated Volume Control)How it Works: Hybrid: set target tidal volume, ventilator adjusts inspiratory pressure breath-to-breath to achieve it (within limits).When It’s Used / Pros: Common default mode on newer vents; combines benefits of VC (guaranteed volume) + PC (pressure limitation).Limitations / Cons: Can increase pressures if compliance worsens.SIMV (Synchronized Intermittent Mandatory Ventilation)How it Works: Delivers set breaths, but allows spontaneous patient breaths in between (without guaranteed volume).When It’s Used / Pros: Used for weaning; allows patient effort.Limitations / Cons: Risk of increased work of breathing if spontaneous breaths are inadequate.PSV (Pressure Support Ventilation)How it Works: Every breath is patient-initiated; ventilator provides preset pressure support to overcome airway resistance.When It’s Used / Pros: Weaning trials; patients with intact drive who just need assistance.Limitations / Cons: Not a full-support mode; not for unstable patients without spontaneous drive. ♟️ Ventilation Strategies Airway ProtectionLow GCS, seizure, strokeLoss of gag/cough reflexHigh aspiration risk (vomiting, GI bleed, poor mental status)Hypoxemic Respiratory FailureSevere pneumoniaARDSPulmonary edemaInhalation injuryVentilatory (Hypercapnic) Failure / Increased Ventilation DemandSevere metabolic acidosis (DKA, sepsis, renal failure) → need high minute ventilationCOPD, asthma (if decompensating)Neuromuscular weakness (myasthenia, Guillain–Barré, spinal cord injury)Airway Obstruction / Anticipated Loss of AirwayTumor, anaphylaxis, angioedemaFacial or airway traumaPre-op / anticipated deterioration Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO) 👤 Show Notes Priyanka Ramesh, MD PGY 1 Internal Medicine Resident Cape Fear Valley Internal Medicine Residency Program Fayetteville NC Aspiring Pulmonary Critical Care Fellow 🔎 Your Deep-Dive Starts Here It seems we can't find what you're looking for. The post REBEL Core Cast 146.0–Ventilators Part 4: Setting up the Ventilator appeared first on REBEL EM - Emergency Medicine Blog.

🧭 REBEL Rundown 📝 Introduction Welcome to the Rebel Core Content Blog, where we delve into crucial knowledge for emergency medicine. Today, we share insightful tips from PEM specialist Dr. Elise Perelman, shedding light on respiratory challenges in infants, toddlers, and young children during the viral season. Understanding that most cases involve typical viruses, we aim to equip you with diagnostic pearls to identify more serious pathologies. Click here for Direct Download of the Podcast. 🔍 Recognizing Respiratory Patterns Pearl #1: Look at Your PatientBegin exams from the doorway. Observing patterns such as accessory muscle usage can reveal a patient’s respiratory effort. Specify whether the work of breathing occurs during inspiration, expiration, or both. Inspiratory work indicates difficulty getting air in, while expiratory work suggests trouble pushing air out. Silent tachypnea may point to other issues, like acidemia or pneumothorax. 🩺 Localizing Sounds for Accurate Diagnosis Pearl #2: Localize the SoundBreathing noises signal varied respiratory issues. Stridor, often heard on inspiration, results from obstructions above the thoracic inlet. Conversely, wheezing, generally linked to exhalation, indicates obstructions in the lower airways. Watch for signs like ‘silent chest’—a dangerous, severe obstruction, and distinguish grunting as a bodily mechanism to prevent alveolar collapse. Correctly identifying the sound assists in determining the appropriate intervention. 💉 Tailoring Treatment for Effective Results Once a sound is localized, treatments vary. We explore Soder from nasal congestion, typically needing supportive care and suctioning. Stridor from conditions like croup is eased with interventions to reduce airway swelling, such as steroids or inhaled epinephrine. Conversely, wheezing in infants is often due to bronchiolitis—not bronchospasms—and over-treatment is to be avoided. Supportive measures including suction, hydration, and oxygen are preferred unless improvement warrants bronchodilators. 🌬️ Intervening with Severe Asthma In severe cases of asthma or bronchiolitis, where standard at-home treatments fail, immediate adjunct therapies like intramuscular epinephrine become essential. Administering this quickly can alleviate obstruction when inhalants aren’t effective due to low air movement. 🦓 Navigating the Zebras of Respiratory Cases When recognizing Zebras—uncommon cases overshadowed by routine diagnoses—remain vigilant for histories or presentations that don’t conform. Conditions like pneumonia, bacterial tracheitis, and even myocarditis may mimic more common issues. 📌 Conclusion As attending physicians, our role extends beyond conventional treatment—it’s about discerning the atypical from the typical. Dr. Perelman urges continual reassessment, emphasizing reliance on observational skills as much as technological aid. Keeping keen on respiratory nuances ensures we catch those outlier cases, paving the way for adept medical care despite the overwhelming prevalence of viral infections.Stay tuned for more pearls and insights in our future posts, as Dr. Perelman shares further strategies for effective pediatric emergency care. For more resources, continue exploring our faculty’s valuable contributions on our site. Until then, stay safe and perceptive in your practice. Post Peer Reviewed By: Mark Ramzy, DO (X: @MRamzyDO), and Marco Propersi, DO (X: @Marco_Propersi) 👤 Guest Elise Perlman MD Pediatric Emergency Medicine​ Assistant Professor, Donald and Barbara Zucker School of Medicine at Hofstra/Northwell Meet The Team 🔎 Your Deep-Dive Starts Here REBEL CAST – RENOVATE Trial: HFNC vs BPAP in Acute Respiratory Failure The RENOVATE trial set out to answer a high-impact question ... Resuscitation Read More REBEL MIND: Performance Under Pressure – What Medicine Can Learn from Elite Teams Welcome back to Rebel MIND, the podcast where we sharpen ... Human Behavior Read More REBEL Core Cast 148.0–Demystifying Non-Invasive Ventilation & HiFlow Non-invasive ventilation (NIV) refers to respiratory support provided without endotracheal ... Thoracic and Respiratory Read More REBEL MIND – The Dunning Kruger Effect: Why Looking Inward Improves Patient Care In this episode and blog post, hosts Mark Ramzy and ... Human Behavior Read More REBEL Core Cast 147.0–Ventilators Part 5: Key Mechanical Ventilator Pressures & Definitions Made Simple This episode reviews essential ventilator pressures and how to interpret ... Thoracic and Respiratory Read More REBEL Core Cast 146.0–Ventilators Part 4: Setting up the Ventilator Ventilator management can feel overwhelming—there are so many knobs to ... Thoracic and Respiratory Read More The post REBEL Core Cast – Pediatric Respi

🧭 REBEL Rundown 📝Introduction Welcome to this special edition of the REBEL Cast, where we unravel key highlights and educational insights from the IncrEMentuM Conference in Spain. This event is a cornerstone for advancing emergency medicine education, drawing esteemed speakers and participants from around the globe. As emergency medicine gains traction in Spain, this conference has become an essential platform for knowledge exchange and professional growth. Today, host Dr. Mark Ramzy shines a spotlight on three distinguished speakers: Dr. Jess Mason, Dr. Tarlan Hedayati, and Dr. Simon Carley, who shared their expertise and experiences at this transformative gathering last spring. Click here for Direct Download of the Podcast. 🤔What's IncrEMentuM? A new conference and a pivotal gathering for emergency medicine professionals worldwide, has become an essential platform for education, collaboration, and advocacy, especially in light of emergency medicine’s recent recognition as a specialty in Spain. The conference is praised for its outstanding production quality, engaging speakers, and its capacity to foster a global community of emergency care professionals. 🦪Pearls from Their IncrEMentuM 2025 Lectures Think about alternative diagnoses that could be driving the patient’s atrial fibrillationMaybe the atrial fibrillation is an adaptive response and slowing them down (whether chemically or electrically) may cause more harm than goodGet in the mental space before having to perform a High Acuity Low Occurrence (HALO) procedure and walk through each of the parts step by stepEMRAP has uploaded the video of the Resuscitative Hysterotomy here (Subscription required to watch)Like many things in critical care, a patient with a severe head injury requires you to do many little things very well (ie. reducing ICP increases by taking off the C-collar if able, positioning the patient appropriately, knowing when to use certain medications) See you in Spain! The upcoming conference aims to gather world-class educators once more and promises an enriching experience for all attendees. Drs. Tarlan Hedayati, Jess Mason and Simon Carley, along with many others, will be there at the event. For more information on the IncrEMentuM Conference and to register, visit their website! See you there! Tarlan Hedayati, MD Vice Chair of Education and Associate Program Director Cook County, Chicago, IL Jess Mason, MD Associate Professor of Emergency Medicine Vanderbilt University, Nashville, TN Simon Carley, MD, PhD Professor of Emergency and Dean of the Royal College of Emergency Medicine Manchester, England 🔎 Your Deep-Dive Starts Here REBEL Core Cast 110.0 – On Shift Learning Pearls Take Home Points: Patients with recent onset atrial fibrillation can ... Read More The post REBEL CAST – IncrEMentuM26 Speaker Spotlight : Drs. Tarlan Hedayati, Jess Mason and Simon Carley appeared first on REBEL EM - Emergency Medicine Blog.

🧭 REBEL Rundown 📌 Key Points 🫀 Prolonged QTc raises risk of torsades de pointes ⏱️ Correct for heart rate: QTc > 440 ms (men) or > 460 ms (women); > 500 ms = high TdP risk.💊 Common culprits: Methadone, ondansetron, macrolides, fluoroquinolones, antipsychotics.🧪 Prevention: Check & replete K, Mg, Ca and avoid QT-prolonging meds when possible.🚑 If TdP develops: Defibrillate + IV magnesium and stop offending agents. Click here for Direct Download of the Podcast. 📝 Introduction The QT interval is a vital part of ECG interpretation, reflecting the heart’s electrical recovery after each beat. When prolonged, it can set the stage for torsades de pointes. Understanding how to measure and correct the QT interval, identify high-risk medications, and act quickly when TdP occurs is essential for every clinician. This guide walks you through the physiology, interpretation, common causes, and emergency management of QTc prolongation to keep your patients safe. 🤔 Definition and Physiology QT evaluation is a fundamental component of EKG analysis. The QT interval reflects the time from ventricular depolarization and contraction through ventricular repolarization and relaxation.Clinically, QT prolongation increases the risk of torsades de pointes (TdP) – a form of polymorphic ventricular tachycardia (a non-perfusing rhythm) that is classically described as a pattern of “twisting points” or alternating amplitudes. This occurs when a premature ventricular contraction leads to an R on T phenomenon during the repolarization period.The differential for QT prolongation is long and varied: congenital long QT, electrolyte disturbances (hypoK, hypoMg, hypoCa), hypothermia, myocardial ischemia, and increased intracranial pressure. Moreover, a whole host of xenobiotics can prolong the QT interval: methadone, anti-microbials, anti-emetics, anti-psychotics, and anti-dysrhythmics. 🧮 ECG Interpretation The QT interval must be interpreted in conjunction with the patient’s heart rate. The QT interval with shorten in the context tachycardia and length in the context of bradycardia. In other words, tachycardia is protective when evaluating the patient with prolonged QT.With that in mind, many EKG machines will calculate a corrected QT interval or QTc. The QTc is a standardized way to account for variations in heart rate so clinicians are able to compared QT intervals at different heart rates over time and thus calculate risk.Generally, a QTc is considered prolonged if greater than 440ms in males or 460ms in females. Once the QTc > 500msec, the risk of TdP increases 2-3 fold.1A variety of different correction formulas exist: Bazett, Fridericia, Hodges, Framingham, Rautaharju.Manually, the QT interval should be measured from the beginning of the QRS complex to the end of the T wave – and thus should be measured in leads where all portions can be visualized, most frequently lead II or V5/V6. Ideally, the QT interval should be average over 3 or more beats.2 To determine the end of the T wave, a tangent line should be drawn through the maximum slope of the T wave – the point at which this line crosses the isoelectric line is the end of the T wave.3 💊 Commonly Used QTc Prolonging Medications Methadone: particularly concerning because not only does it inherently prolong QT but also induces a bradycardiaAntiemetics: OndansetronMacrolides: azithromycin, erythromycin, clarithromycinFluroquinolones: ciprofloxacin, levofloxacinAntipsychotics: Haloperidol, Olanzapine ️ Management Prevention is key!Assess electrolytes (Mg, Ca, K) and replete as neededTelemetry MonitoringIf patient happens to fall into TdP, initiate ACLS with immediate defibrillation and magnesium.Withdrawal of offending agents. 📚 References Drew BJ, Ackerman MJ, Funk M, Gibler WB, Kligfield P, Menon V, Philippides GJ, Roden DM, Zareba W. Prevention of torsade de pointes in hospital settings: a scientific statement from the American Heart Association and the American College of Cardiology Foundation. Circulation. 2010 Mar;121(8):1047-1060.Postema PG and Wilde AAM. The measurement of the QT interval. Curr Cardiol Rev. 2014 Aug;10(3): 287-294.https://litfl.com/qt-interval-ecg-library/ Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO) 👤 Associate Editor Anand Swaminathan MD, MPH All Things REBEL EM Meet The Team 🔎 Your Deep-Dive Starts Here REBEL Core Cast 134.0 – Acetaminophen Toxicity Acetaminophen (APAP) overdose remains one of the most common causes ... Toxicology Read More Street Medicine: Compassionate Care for the Unhoused Introduction: In this episode of Rebel Cast, host Marco Propersi, ... Read More REBEL Cast Ep91: Static Ultrasound vs Landmark Placement of Subclavian Central Lines Background Information: Central venous catheterizat

🧭 REBEL Rundown 📌 Key Points 🩸 Tourniquets save lives and limbs: Apply immediately when you’ve got arterial bleeding.📍 Placement matters: Position the tourniquet 5–6 cm proximal to the arterial bleed, or if you can’t identify the exact source, place it as high up on the limb as possible.🔧 Windlass technique: The windlass provides only a small amount of extra pressure. Tighten the velcro first, then twist the windlass 1–2 turns to complete compression. Click here for Direct Download of the Podcast. ⏰ Highlights 00:00 Introduction to Tourniquets00:40 Optimal Placement of Tourniquets01:21 Proper Tightening Techniques01:57 Importance of Timing and Application02:36 Summary and Conclusion 📝 Introduction In this episode of the Rebel Core Content podcast, Swami provides crucial tips on using tourniquets. Highlighting the significance of these life and limb-saving devices, the discussion focuses on the optimal placement of tourniquets, emphasizing placing them 2-3 inches (5-6 cm) above the bleeding source and avoiding joints. Swami also advises on the correct way to tighten the tourniquet using the Velcro strap first, followed by minimal use of the windless. The importance of noting the application time to avoid prolonged arterial flow interruption is also discussed. The episode concludes with a reminder to visit the podcast’s website for more valuable content. Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO) 👤 Associate Editor Anand Swaminathan MD, MPH All Things REBEL EM Meet The Team 🔎 Your Deep-Dive Starts Here REBEL Cast Ep 43: Pain Control and Opioid Sparing Options in the ED Background: In the United States we are not only seeing ... Trauma Read More REBEL Cast Episode 42: Research From the Past Year – In the Pipeline Welcome back to Episode 42 of REBEL Cast. In this ... Read More REBEL Cast Episode 41: Research From the Past Year – Resuscitation Welcome back to Episode 41 of REBEL Cast. In this ... Read More REBEL Cast Episode 40: Research From the Past Year – Pain Control Welcome back to Episode 40 of REBEL Cast. We have ... Trauma Read More February 2017 REBEL Cast: The All Hyperoxia Edition Background: Many providers and health care workers place oxygen on ... Resuscitation Read More REBEL Cast Episode 29: IDSA Pneumonia Update Every few years we get updates in the guidelines based ... Infectious Disease Read More The post REBEL Core Cast 144.0: Tourniquet Tips appeared first on REBEL EM - Emergency Medicine Blog.

🧭 REBEL Rundown 📝Introduction In this exciting episode of REBEL Cast, host Dr. Mark Ramzy joins forces with renowned educator and speaker, Dr. George Willis. Broadcasting straight from the ACEP 25 in Salt Lake City, the duo talk about bringing together the international emergency medicine community, as they reflect on their experiences at the Increment Conference in Murcia, Spain, and preview the upcoming event this spring. Click here for Direct Download of the Podcast. 🤔What's IncrEMentuM? A new conference and a pivotal gathering for emergency medicine professionals worldwide, has become an essential platform for education, collaboration, and advocacy, especially in light of emergency medicine’s recent recognition as a specialty in Spain. The conference is praised for its outstanding production quality, engaging speakers, and its capacity to foster a global community of emergency care professionals. 🦪Pearls from George's IncrEMentuM 2025 Lectures: Sodium Bicarbonate Use:Appropriate Use: Focus on specific instances like metabolic acidosis with renal failure or severe metabolic cases with tox patients (e.g., salicylate or TCA overdose).Emphasis on Patient-Centric Care: Treat the patient, not the number; avoid harmful overreliance on bicarb based solely on lab resultsDiabetic Ketoacidosis (DKA):Balanced Solutions: Preferenced over normal saline to prevent hyperchloremic acidosis.Potassium Management: Oral potassium is effective and should be utilized, challenging the myth of impaired gastric absorption in DKA.Squid Protocol: Usage of ultra-rapid insulin subcutaneously as an alternative to insulin drips in mild to moderate DKA cases.We covered this topic before on REBEL EM. Check out the post here and the podcast hereCrashing Aortic Dissection:Hypotension Insights: Do not attribute sudden hypotension solely to medication; prioritize ruling out tamponade or cardiogenic shock.Ultrasound Utilization: Essential tool for detecting complications like tamponade or low EF due to myocardial infarction or aortic valve regurgitation.Controlled Pericardial Drainage: Crucial technique to stabilize hemodynamics without increasing mortality, avoiding extensive fluid removal.Here’s a helpful algorithmic infographic to reference for aortic dissection patients:Image Courtesy of Dr. Mark Ramzy, DO (@MRamzyDO) HyperkalemiaNot every patient needs calcium. Dont just give it prophylatically, only those with EKG changes should get it and get enough of it.Give an appropriate dose of your other medications. That includes giving 10 units of insulin and 2 amps of dextrose 50. One when they get the 10 units of insulin and the other 30 minutes laterPatients may be dehydrated, dont give them furosemide or diuretics. Those patients need fluid to help perfuse their kidneys and eliminate potassiumHere’s the Algorithm George mentioned in the episodeHere’s a REBEL REVIEW breaking down the different electrolytes in each of the types of fluids: 🫣Teasers from George's IncrEMentuM 2026 Lectures: Severe Thyroid Storm:Diagnosis Reminder: Consider thyroid storm in febrile patients with altered mental status; order TSH tests.Beta Blocker Administration: Use ultrasound to assess heart function before administering propranolol to prevent low output heart failure.Medication Timing: Administer iodine after antithyroid drugs.Refractory Hypoglycemia:Early Use of Octreotide: Beneficial in sulfonylurea-induced cases; initiate treatment promptly for better efficacy.Broadened Perspective: Consider other endocrine disorders as potential causes beyond typical measures.Modern Management of SCAPE:Bolus Dose Nitroglycerin: A recommended practice for quick patient stabilization and improved outcomes in SCAPE scenarios.We covered this topic before on REBEL EM, see Dr. Marco Propersi’s post here See you in Spain!  The upcoming conference aims to gather world-class educators once more and promises an enriching experience for all attendees. George Willis, along with many others, will bring significant discourse to the event. For more information on the IncrEMentuM Conference and to register, visit their website! See you there! Mark Ramzy, DO Co-Editor-in-Chief RWJBH / Rutgers Health, Newark NJ George Willis, MD Vice Chair and Assistant Program Director UT Health, San Antonio, TX 🔎 Your Deep-Dive Starts Here REBEL Core Cast – DKA: Beyond the Basics Part 2 – SCOPE DKA-Trial Managing diabetic ketoacidosis (DKA) requires careful consideration of fluid therapy, ... Endocrine, Metabolic, Fluid, and Electrolytes Read More REBEL Core Cast – DKA: Beyond the Basics Part 1 – The SQuID Protocol In this episode of REBEL Cast, we dive into part ... Endocrine, Metabolic, Fluid, and Electrolytes Read More REBEL Core Cast 18.0 – DKA Tips and Tricks Take Home Points When looking at pH and bicarb, the ... Endocrine, Metabolic, Fluid, and Electrolytes Read More The post R

🧭 REBEL Rundown 🔑Key Points 💧 Fluid Choice Matters: Plasma-Lyte, a balanced crystalloid, corrected acidosis faster than normal saline in severe DKA patients, with no increase in adverse events.🧪 Chloride Load Concerns: Normal saline’s high chloride content can worsen acidosis, potentially slowing bicarb recovery even after the anion gap closes.🔬 Study Design Strengths: The SCOPE-DKA trial was a cluster crossover, open-label RCT, protocolizing all variables except fluid type, enhancing the reliability of its findings.🧮 Base Excess & Strong Ion Difference: Base excess/deficit and strong ion difference are valuable but underutilized tools for assessing acid-base status—don’t rely solely on pH or bicarb.⚠️ Limitations & Next Steps: The study did not include lactated Ringer’s, and fluid rates were left to clinical discretion. More research, including three-arm trials, is needed for definitive guidance. Click here for Direct Download of the Podcast. 📝 Introduction Managing diabetic ketoacidosis (DKA) requires careful consideration of fluid therapy, especially in severe cases. In part two of our REBEL Cast DKA series, we shifted from insulin strategies to fluid choice in severe DKA, diving into the SCOPE-DKA trial—a cluster, crossover, open-label RCT from Australia. While normal saline (NS) is commonly used, concerns about its high chloride content and impact on acidosis have sparked growing interest in balanced solutions like Plasma-Lyte. Clinical Question Does the fluid you choose affect how quickly acidosis resolves in DKA?  IV Fluid Composition 🚨 Clinical Bottom Line Plasma-Lyte showed a modest but meaningful benefit over normal saline in resolving metabolic acidosis in patients with severe DKA. Though safety profiles were similar, the more balanced electrolyte composition of Plasma-Lyte helped normalize acid-base status slightly faster—without worsening ketosis. While this won’t revolutionize care overnight, it’s one more step toward physiologic resuscitation in DKA. Understanding fluid composition and its impact on acid-base balance is crucial for optimal patient care. Post Peer Reviewed By: Marco Propersi (Twitter/X: @Marco_propersi), and Kim Bambach, MDShow Notes By: Mark Ramzy, DO Authors Mark Ramzy, DO Co-Editor-in-Chief RWJBH / Rutgers Health, Newark, NJ Frank Lodeserto Associate Editor Cape Fear Valley Medical Center, Fayetteville NC 🔎 Your Deep-Dive Starts Here It seems we can't find what you're looking for. REBEL Castis the blogs audio version. The podcast typically starts by setting a clinical stage with a pertinent clinical question, followed by a discussion of the paper with pertinent results, strengths, limitations, and further discussion. Finally, we end every podcast with clinical take home points from the papers being reviewed. If there are papers you think we should evaluate, email them to [email protected]. REBEL EM stands for Rational Evidence Based Evaluation of Literature in Emergency Medicine.  We cover a myriad of topics, primarily focusing on evidence-based clinical topics.At its core, evidence-based medicine (EBM) incorporates clinical judgment, relevant scientific evidence, and patient values/preferences. Research and scientific evidence help inform care but should not dictate care of patients.With the constant influx of new published research, it makes it difficult to stay current with the latest and greatest. REBEL EM was created October 2013 in an effort to cut down knowledge translation of research to clinical application (Bench to Bedside), using a structured critical appraisal method of evaluation. REBEL Core Cast – DKA: Beyond the Basics Part 2 – SCOPE DKA-Trial Mark Ramzy October 21, 2025 No Comments Managing diabetic ketoacidosis (DKA) requires careful consideration of fluid therapy, especially in severe cases. In part two of our REBEL Cast DKA series, we shifted from insulin strategies to fluid choice in severe DKA, diving into the SCOPE-DKA trial—a cluster, crossover, open-label RCT from Australia. While normal saline (NS) is commonly used, concerns about its high chloride content and impact on acidosis have sparked growing interest in balanced solutions like Plasma-Lyte. Read More » « Page1 Page2 Page3 Page4 Page5 » The post REBEL Core Cast – DKA: Beyond the Basics Part 2 – SCOPE DKA-Trial appeared first on REBEL EM - Emergency Medicine Blog.

🧭 REBEL Rundown 🗝️ Key Points 🛏️ Fewer ICU AdmissionsOnly 5 patients in the SQuID group required ICU care vs 99 in the traditional insulin drip group.⏱️ Shorter ED StaysED length of stay dropped by ~3 hours in the SQuID group—an operational win in crowded departments.💉 No Drop in Nursing WorkloadDespite using subQ insulin, nurses still performed hourly glucose checks and frequent injections.🧪 Focus on the Anion GapDKA resolution = closing the anion gap, not just normalizing blood sugar—critical concept for trainees and nurses alike.👶 Peds Has the EdgePediatric ICUs routinely use a 2-bag system (D10 + electrolytes vs electrolytes alone) to safely continue insulin while managing glucose—adult medicine should take note. Click here for Direct Download of the Podcast. 📝 Introduction In this episode of REBEL Cast, we dive into part one of our Diabetic Ketoacidosis (DKA) series with a twist—subcutaneous insulin instead of the traditional IV drip. We explore the SQuID Protocol (Subcutaneous Insulin in DKA), which could potentially shift how we manage mild to moderate DKA—from the ICU to the general floor.With ICU bed shortages, ED boarding, and nursing resource challenges, it’s time to ask: Do all DKA patients really need a drip and an ICU bed?We reviewed a quasi-experimental study comparing traditional insulin drips versus subcutaneous insulin (lispro q4h + glargine at time zero) in a busy urban ED. The results? Promising—but not without caveats. 🦑 SQuID Protocol 🚨 Clinical Bottom Line The SQuID Protocol appears safe and effective for carefully selected patients with mild to moderate DKA. It may reduce ICU admissions and shorten ED stays. But implementation requires thoughtful coordination, nursing comfort, and institutional buy-in. This isn’t ready for prime time everywhere—but it’s worth knowing and considering when ICU resources are tight. Post Peer Reviewed By: Marco Propersi (Twitter/X: @Marco_propersi), and Kim Bambach, MDShow Notes By: Mark Ramzy, DO Authors Mark Ramzy, DO Co-Editor-in-Chief RWJBH / Rutgers Health, Newark, NJ Frank Lodeserto Associate Editor Cape Fear Valley Medical Center, Fayetteville NC 🔎 Your Deep-Dive Starts Here It seems we can't find what you're looking for. The post REBEL Core Cast – DKA: Beyond the Basics Part 1 – The SQuID Protocol appeared first on REBEL EM - Emergency Medicine Blog.

🧭 REBEL Rundown 🗝️ Key Points ❌ Don’t chase perfect numbers: Adequate and safe is often better than “perfect but harmful.”💨 Oxygenation levers: Start with FiO₂ and PEEP, but remember MAP is the true driver.🫁 Ventilation levers: Adjust RR and TV, tailored to underlying physiology.🚫 Watch your obstructive patients: Sometimes less RR is more. Click here for Direct Download of the Podcast. 📝 Introduction When you take the airway, you take the wheel and you now control the patient’s oxygenation and ventilation. In this REBEL Crit episode, Dr. Lodeserto and Dr. Acker walk through the physiology, ventilator strategies, and clinical curveballs that separate calm control from chaos at the bedside. ️ The Two Pillars of Vent Management 1. Oxygenation — Getting O₂ InPrimary levers: FiO₂ (fraction of inspired oxygen) and PEEP (positive end-expiratory pressure).Real driver: Mean Airway Pressure (MAP) :  the average pressure applied to the lungs across the entire respiratory cycle.Key physiology:Oxygen enters blood by diffusion down a concentration gradient.Adequate alveolar surface area is critical → PEEP keeps alveoli open, prevents collapse/reopen injury, and ensures FiO₂ delivery actually translates into effective oxygenation.MAP analogy: Just as mean arterial pressure drives perfusion, mean airway pressure drives oxygenation. Prolonged inspiratory time or sustained pressure (e.g., APRV, inverse I:E) can raise MAP.Risks: Excessive pressure/volume can cause barotrauma or volutrauma. 2. Ventilation — Getting CO₂ OutPrimary levers: Tidal Volume (TV) and Respiratory Rate (RR).Minute Ventilation = RR × TV.Mechanism: Ventilation removes CO₂ through bulk convection (movement of air in and out).Disease-specific strategies:Obstructive Disease (COPD / Asthma)RR ↓ to allow more time for exhalation.Ensure expiratory flow = inspiratory flow → prevents air trapping.If not equal → auto-PEEP → increased intrathoracic pressure → ↓ preload, risk of hypotension, cardiac arrest, or pneumothorax.Metabolic AcidosisRR ↑ to blow off CO₂ and buffer acidosis.ARDSTidal volume limited to 4–6 mL/kg IBW to minimize ventilator-induced lung injury.RR becomes the main adjustment knob.Exception: in obstructive lung disease, patients need extra time to exhale (I:E may be 1:4–1:6). 💡 Why This Matters Ventilator management is part science, part art. Understanding the physiology and knowing when to bend or break the rules  helps protect patients from ventilator-induced injury and improves outcomes. Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)Show Notes By: Rubén Tapia-Bucheli, M.D. 👤 Guest Contributors Rubén Tapia-Bucheli, M.D. 3rd Year Internal Medicine Resident Cape Fear Valley Internal Medicine Residency Program Fayetteville NC Aspiring Pulmonary Critical Care Fellow 🔎 Your Deep-Dive Starts Here It seems we can't find what you're looking for. The post REBEL Core Cast 143.0–Ventilators Part 3: Oxygenation & Ventilation — Mastering the Balance on the Ventilator appeared first on REBEL EM - Emergency Medicine Blog.

🧭 REBEL Rundown 🗝️ Key Points 💨 Start with Breath Types: Controlled, assisted, and supported breaths are the foundation of all modes.🛌 Comfort Over “Best Mode”: No mode improves mortality — focus on patient synchrony and comfort. Know the Big 5 Modes: AC: All controlled or assisted (volume or pressure). PS: Fully spontaneous, great for SBTs. PRVC: Pressure-delivered, volume-targeted hybrid. SIMV: Mixed mode, less favored in adults. VS: Spontaneous mode with adaptive pressure.⚠️ Watch for Pitfalls: PRVC may under-ventilate in agitation. SIMV often causes dyssynchrony.🎯 Bottom Line: Master mode mechanics and match the vent to the patient — not the other way around. Click here for Direct Download of the Podcast. 📝 Introduction Mechanical ventilation can feel overwhelming, especially when faced with a sea of ventilator modes and unfamiliar terminology. In Part 2 of the series, we go beyond breath types and delivery mechanics to explore the most used modes in the ICU. We will break down each one; explaining how it works, when to use it, and why the goal isn’t the “best mode” but the most comfortable one for the patient. ️ Ventilator Modes Explained Assist Control (AC)Commonly mislabeled as “volume control” or “pressure control.”Two main types:AC Volume: Delivers a preset tidal volume with each breath, whether machine-initiated (controlled) or patient-initiated (assisted).AC Pressure: Delivers a preset pressure; tidal volume varies based on compliance.All breaths are either controlled or assisted. Pressure Support (PS)All breaths are spontaneous initiated by the patient.The ventilator provides a preset level of pressure support, like a resistance band during a pull-up.No set rate, but a backup mode (often AC) activates during apnea.Commonly used for spontaneous breathing trials (SBTs) to assess extubation readiness.Typical goal: Patient breathing comfortably with PS ~5 cmH₂O and reasonable rate. Pressure Regulated Volume Control (PRVC)Also called autoflow or adaptive pressure ventilation.A hybrid mode: Pressure-delivered, volume-targeted.Delivers breaths with a decelerating flow waveform, mimicking physiologic breathing.Adjusts pressure breath-to-breath to meet a target tidal volume with minimal required pressure.Safety feature: Pressure limit (e.g., 30–35 cm H₂O). If exceeded, volume delivery stops early.Pitfall: In agitated patients, rapid breathing may trick the ventilator into reducing pressure, causing under-ventilation. Synchronized Intermittent Mandatory Ventilation (SIMV)Less common in adult ICU but still commonly used in pediatrics.Delivers a set number of mandatory (controlled or assisted) breaths.Allows spontaneous, pressure-supported breaths between mandatory ones.Example: SIMV 10 = 10 guaranteed AC breaths; additional breaths are spontaneous + supported.Why it’s less popular: Found to be less effective than daily SBTs for weaning and frequent dyssynchrony from not giving enough PS (PS should target at least  2/3 of the AC breath volumes) . Volume Support (VS)A newer, fully spontaneous mode (like PS + PRVC).Patient initiates all breaths.The ventilator automatically adjusts pressure support to achieve a target tidal volume.Think of it as the spontaneous cousin of PRVC—adaptive and volume-driven. 🚨 Clinical Bottom Line Understanding ventilator modes starts with knowing breath types, delivery mechanics, and clinical goals. When it comes to choosing the right mode:Focus less on the “best” mode and more on patient comfort and synchrony.Recognize the strengths, limitations, and pitfalls of each mode.Stay tuned for future episodes that dive into ventilator troubleshooting and advanced respiratory strategies. Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)Show Notes By: Nicole Ebalo, DO 👤 Guest Contributors Eric Acker, MD Internal Medicine, Chief Resident, Cape Fear Valley Medical Center, Fayetteville NC Nicole Ebalo, DO Internal Medicine, Chief Resident, Cape Fear Valley Medical Center, Fayetteville NC 🔎 Your Deep-Dive Starts Here It seems we can't find what you're looking for. The post REBEL Core Cast 142.0–Ventilators Part 2: Simplifying Mechanical Ventilation – Most Common Ventilator Modes appeared first on REBEL EM - Emergency Medicine Blog.

🧭 REBEL Rundown Click here for Direct Download of the Podcast. ⏰ Highlights 00:00 Introduction to Rebel Cast00:10 Highlighting the Incrementum Conference 202600:34 Meet the Founders of Incrementum01:21 The Journey to Incrementum04:27 The Recognition of Emergency Medicine in Spain06:04 What is Incrementum?08:14 Bringing Together Top Emergency Medicine Experts11:38 Exciting Sessions to Look Forward To15:54 Conclusion and Invitation to Incrementum 2026 📝 Introduction In this special episode of Rebel Cast, we spotlight the Incrementum Conference in Spain, a significant event in emergency medicine. Hosts welcome Dr. Francisco ‘Paco’ Campillo Palma and Dr. Carmen Maria Cano, founders of Incrementum, to discuss the recognition of emergency medicine as a specialty in Spain. They share their journey of creating the conference, emphasizing the importance of education, collaboration, and growth. The discussion also touches on this year’s conference highlights, including sessions on mental health and evidence-based medicine, and the exceptional lineup of speakers. Listeners are encouraged to attend the conference in April 2026 for an enriching experience. 📌 Bottom Line Join us in Spain this April for the Increment Conference!👉 Register now at incrementum-conference.com Post Peer Reviewed By: Mark Ramzy, DO (X: @MRamzyDO) 👤 Co-Editor-In-Chief Marco Propersi DO All Things REBEL EM Meet The Team 🔎 Your Deep-Dive Starts Here REBEL Core Cast 145.0: Understanding QTc Prolongation: Causes, Risks, and Management The QT interval is a vital part of ECG interpretation, ... Procedures and Skills Read More REBEL Core Cast 144.0: Tourniquet Tips In this episode of the Rebel Core Content podcast, Swami ... Procedures and Skills Read More REBEL Core Cast 138.0: A Simple Bedside Approach to Shock In this episode, we will dive into a simple yet ... Cardiovascular Read More REBEL Core Cast 131.0 – Traumatic Arthrotomy Take Home points: Always suspect an open joint if there ... Trauma Read More REBEL Core Cast 130.0 – Omphalitis Take Home Points Early diagnosis: erythema and warmth of the ... Pediatrics Read More REBEL Core Cast 129.0 – Gastric Lavage Take Home Points Orogastric lavage may still play an important ... Toxicology Read More The post Incrementum Conference 2026: Revolutionizing Emergency Medicine in Spain appeared first on REBEL EM - Emergency Medicine Blog.

🧭 REBEL Rundown 🗝️ Key Points 💨 Master the 3 Types of BreathsControl, Assist, and Spontaneous — know the difference before tackling ventilator modes.📦 Breath Delivery: Volume vs. PressureVolume-Targeted = fixed volume → monitor pressure📈 Pressure-Targeted = fixed pressure → monitor volume🫁 Lung Compliance = Pressure-Volume RelationshipVolume mode: ↑ pressure = ↓ compliance (stiff lungs)Pressure mode: ↓ tidal volume = ↓ compliance Click here for Direct Download of the Podcast. 📝 Introduction For many medical residents, the ICU can feel like stepping into a pressure cooker. At the heart of that stress often lies one intimidating machine: the ventilator. Rather than diving headfirst into complex ventilator modes, this episode lays a critical foundation by breaking down the basic building blocks of mechanical ventilation, something every clinician should master before moving on to more advanced concepts. Once you know the 3 types of breaths and how those breaths are delivered, you can more easily understand most of the mechanical ventilator modes.  🧮 The 3 Types of Breaths To simplify things, we use a pull-up analogy to explain the types of ventilator breaths: 🫁 The 3 Types of Breaths…It's Like 😮‍💨 Breath Delivery: Volume vs. Pressure Once you know the type of breath, the next key concept is how it’s delivered:1. Volume-Targeted DeliveryThe ventilator delivers a fixed tidal volume (e.g., 400 mL) with each control or assist breath.What to monitor: Pressure. As lung compliance worsens, pressure increases.Risk: Barotrauma if the pressure becomes too high.2. Pressure-Targeted DeliveryThe ventilator delivers air to a preset pressure (e.g., 15 cm H₂O).What to monitor: Tidal volume. As compliance drops, so does delivered volume.Adjustment: Modify pressure to maintain appropriate ventilation. 🧱 Putting It All Together: Lung Compliance The relationship between pressure and volume is described by compliance:📐 Compliance = Δ Volume / Δ PressureIn volume mode:Rising pressure to achieve the same volume = decreased compliance (stiff)Decreasing pressure to achieve the same volume = increased compliance (loose)In pressure mode:Dropping tidal volume at a constant pressure = decreased compliance (stiff)Rising tidal volume at a constant pressure = increased compliance (loose) 🚨 Clinical Bottom Line Before tackling advanced ventilator modes, master these foundational concepts:The three breath typesThe two delivery methodsThe role of lung complianceOnce you’ve got these down, the rest of mechanical ventilation becomes far easier to understand.Stay tuned for Part 2, where we’ll build on this foundation and unpack the most commonly used ventilator modes. Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO)Show Notes By: Nicole Ebalo, DO 👤 Guest Contributors Eric Acker, MD Internal Medicine, Chief Resident, Cape Fear Valley Medical Center, Fayetteville NC Nicole Ebalo, DO Internal Medicine, Chief Resident, Cape Fear Valley Medical Center, Fayetteville NC 🔎 Your Deep-Dive Starts Here It seems we can't find what you're looking for. The post REBEL Core Cast 141.0–Ventilators Part 1: Simplifying Mechanical Ventilation — Types of Breathes appeared first on REBEL EM - Emergency Medicine Blog.

🧭 REBEL Rundown 📌 Key Points 💉 IO Lines Are Life-Saving in Extremis: IO access is fast, reliable, and can deliver nearly any resuscitative medication or fluid during cardiac arrest or hemorrhagic shock.🧭 Location Matters for Flow. Sternal IO: 💨 Fastest (up to 500cc/5 min). Humerus IO: ⚡ Faster than tibia (300cc/5 min). Tibial IO: 🐢 Slower (200cc/5 min) but easier to place during CPR⚠️ Watch for Contraindications: Avoid IO placement in bones with fractures, prior IO attempts, or compromised circulation proximal to the site.🩸 Labs From IO = ❌: Labs drawn from IO lines are generally unreliable. Once stabilized, obtain bloodwork through IV access.🎯 Stabilize or Lose It: IO dislodgement is common—always use a stabilizer or secure with gauze and tape if none is provided.🧠 Don’t Forget Non-Trauma Uses: IO isn’t just for trauma—think about it in medical arrests, shocked pediatric patients, and patients with difficult IV access. Click here for Direct Download of the Podcast. ⏰ Highlights 00:00 Introduction to the Podcast00:07 First Encounter with Intraosseous Lines01:09 Advantages of Intraosseous Lines02:42 Intraosseous Lines in Pediatric Patients03:34 Optimal Locations for Intraosseous Lines06:17 Limitations and Considerations07:34 Conclusion and Final Thoughts 📝 Introduction Welcome to the Rebel Core Content blog, your go-to source for core medical concepts applicable to practitioners anywhere, anytime. Today, we delve into the world of Intraosseous (IO) lines—a crucial tool in emergency medicine. Swami shares insights into the effectiveness and limitations of IO usage in diverse clinical scenarios. 🧠 Background The sicker the patient, the more likely an IO line is the right choice. In emergencies such as cardiac arrest or hemorrhagic shock, the speed and reliability of IO access outshine traditional intravenous (IV) or central line placements. There’s virtually no resuscitation medication or blood product that cannot be administered through an IO, making it indispensable in life-threatening situations. 🧭 Location While proximal humerus site portents faster infusion rates than proximal tibia site, the main limitation of the proximal humerus site is that the arm must be held in internal rotation to avoid dislodgement of the IOProximal tibia may be easier to landmark than proximal humerusOther sites include distal tibia, distal femur and sternum but are uncommonly employed in EDs 🚰 Flow Rates Proximal Humerus IO~300cc over 5 minutesFaster than tibiaMay be harder to access in some trauma or positioning scenarios Tibial IO~200cc over 5 minutesSlower flow compared to humerusEasier to access, especially during CPR or transport Sternal IOUp to 500cc over 5 minutesHighest flow rateBest for rapid volume resuscitationRisk of dislodgement or interfering with CPR compressions ⚠️ Limitations Placing an IO in a bone with a proximal fracture, a previous IO placement attempt or any circulatory compromise proximal to the site is contraindicatedBlood work drawn from an IO are generally not accurate, so once the patient has been resuscitated with the IO, intravenous blood draws are recommendedDislodgement is common; it is best to use the stabilizer that comes with the IO kit; if the kit does not have a stabilizer, stack lots of gauze on both sides of the IO needle and tape it down 🚨 Clinical Bottom Line Intraosseous lines are a powerful tool, particularly in acute resuscitation scenarios involving cardiac arrest or severe trauma. While they offer quick and effective access, Clinicians must remain vigilant about their limitations and be prepared to switch to more stable options as patients stabilize. Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO) 👤 Associate Editor Anand Swaminathan MD, MPH All Things REBEL EM Meet The Team 🔎 Your Deep-Dive Starts Here REBEL Cast Episode 28: Refractory Ventricular Fibrillation Background: Welcome back to the September 2016 REBEL Cast. We ... Cardiovascular Read More REBEL Cast Episode 27: The PROCAMIO Trial – IV Procainamide vs IV Amiodarone for the Acute Treatment of Stable Wide Complex Tachycardia Background: In the ACLS guidelines stable Ventricular Tachycardia (VT) can ... Cardiovascular Read More REBEL Cast Episode 26: Advice to the Graduating Resident – Victoria Brazil So this is the third installation of Advice to the Graduating ... Read More REBEL Cast Episode 24: Advice to the Graduating Resident – Amal Mattu So this is the second installation of Advice to Graduating ... Read More REBEL Cast Episode 23: Is ST-Segment Elevation in Lead aVR Getting Too Much Respect? with Amal Mattu Lead aVR is a commonly ignored lead and I have ... Cardiovascular Read Mor

🧭 REBEL Rundown 📌 Key Points 🧠 Think Beyond Trauma: Don’t forget to suspect tension pneumothorax in ventilated patients who suddenly crash or after a central line placement! 🫁⚠️🔍 Confirm with Ultrasound: If the patient is stable enough, grab the probe! 🖐️📟Ultrasound can rapidly confirm tension PTX and avoid unnecessary delays.💉🚫 Needles Are Out: Needle decompression? Meh. Finger thoracostomy is faster, more reliable, and more definitive. 🖐️🫁  Click here for Direct Download of the Podcast. 📝 Introduction On this episode of the Rebel Core Cast, Swami takes a deep dive into pneumothorax decompression, focusing on the need for improvements beyond the classic teachings. Covering scenarios where immediate decompression is critical, particularly in tension pneumothorax, Swami discusses the limitations of needle decompression, especially in the second intercostal space at the midclavicular line. He highlights the importance of using POCUS for diagnosis and recommends skipping needle decompression in favor of finger thoracostomy for a more reliable and effective treatment. Key takeaways emphasize recognizing tension pneumothorax in various clinical situations and the advantages of finger thoracostomy over traditional techniques. ⏰ Highlights 00:00 Introduction to Pneumothorax Decompression00:17 Recognizing Tension Pneumothorax01:00 Common Scenarios for Pneumothorax01:34 Confirming Diagnosis with POCUS01:50 Issues with Needle Decompression03:21 Advantages of Finger Thoracostomy04:11 Key Takeaways and Conclusion 📚 References Ferrie EP et al. The right place in the right space? Awareness of site for needle thoracentesis. Emerg Med J 2005; 22: 788-9 PMID: 16244336Laan DV et al. Chest wall thickness and decompression failure: a systematic review and meta-analysis comparing anatomic locations in needle thoracostomy. Injury; 2016; 47(4): 797-804 PMID: 26724173Terboven T et al. Chest wall thickness and depth to vital structures in paediatric patients – implications for prehospital needle decompression of tension pneumothorax. Scan J Trauma Resusc Emerg Med 2109; 27(1). PMID: 30992028 Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO) 👤 Associate Editor Anand Swaminathan MD, MPH All Things REBEL EM Meet The Team 🔎 Your Deep-Dive Starts Here REBEL Cast Episode 20: All Cardiology Episode Welcome to the December 2015 REBELCast, where Swami, Matt, and I ... Cardiovascular Read More REBEL Cast Episode 17: The All Thoracotomy Episode Welcome to the October 2015 REBELCast, where Swami, Matt, and I ... Resuscitation Read More REBEL Cast Episode 15: MET for Renal Colic & Use of Broselow Tape to Estimate Pediatric Weights Welcome to the August 2015 REBEL Cast, where Swami, Matt, and I ... Pediatrics Read More REBEL Cast Episode 14: Early Cardiac Catheterization in OHCA Survivors with Non-STEMI Background: We know that cardiac arrest is a devastating disease ... Cardiovascular Read More REBEL Cast Episode 12: Bootcamp Edition – Delayed Sequence Intubation Welcome back to a special edition, or should I say ... Resuscitation Read More REBEL Cast Episode 10: Corticosteroids in Allergic Reactions/Anaphylaxis & Age of PRBCs in Critically Ill Adults Welcome to the May 2015 REBELCast, where Swami, Matt, and I ... Allergy and Immunology Read More The post REBEL Core Cast 139.0: Pneumothorax Decompression appeared first on REBEL EM - Emergency Medicine Blog.

🧭 REBEL Rundown 📌 Key Points 🧠 Shock is a Clinical Diagnosis — Not Just a NumberPatients can be in compensated shock with normal BP. Look for signs like AMS, cool extremities, ↓ UOP, and ↑ HR/RR.🖐️ Start with the 4 L’sLucid (mental status), Limbs (warm/cold), Leak (urine output), and Lactate give you rapid bedside insight into perfusion status.💡 Pulse Pressure Helps Pinpoint the Type➡️ Narrow PP = Cardiogenic, Hypovolemic, or Obstructive shock➡️ Wide PP = Distributive shock (Sepsis, Anaphylaxis, Neurogenic)🚨 Be Systematic at the BedsideQuick vitals, focused history, and targeted exam can reveal the etiology faster than invasive tools. Click here for Direct Download of the Podcast. 📝 Introduction In this episode, we will dive into a simple yet effective bedside approach to a patient in shock. By using quick physical exam findings and bedside vitals (particularly pulse pressure), you can form a quick assessment of the likely underlying etiology of a critically ill patient.  🔑 Key Concepts What is Shock? Supply vs. Demand mismatch:Inadequate perfusion relative to metabolic demandsLeading to tissue hypoxia and cell death DO2 = CO x (Hb x Sat + (0.003 x paO2))CO = Heart Rate x Stroke VolumeDeterminants of Stroke Volume: Preload, Contractility, and Afterload 4 L’s of Hypotension Lucid: What’s their mental status?Limbs: Are they cold vs. warm? What is the cap refill?Leak: Are they taking a “leak”? What is the urine output? Lactate Remember: Shock DOES NOT equal hypotension A patient in shock can still have normotensive pressures in “Compensated Shock”Signs of ShockIncreased HR, increased RR, AMS, decreased urine output, cool to touch, weak pulses, slow capillary refill Defining Blood Pressure Systolic Blood Pressure Stroke Volume: Main contributor to SBP ➡️ SV ≈ SBP Aortic/Arterial Compliance Diastolic Blood Pressure Systemic Vascular Resistance Maintains end-organ perfusion in diastole Pulse PressureSBP – DBP Mean Arterial Pressure MAP < 60-65 can lead to end-organ damage  Narrow Pulse Pressure Cardiogenic: “Cold Shock”Low contractility ➡️low SV ➡️ low SBP ➡️ increased HR + increased SVR due to catecholamine release leading to increased DBP Cold limbs, weak pulses, poor capillary refill  Hypovolemic Hemorrhagic vs. Dehydration Decrease preload ➡️ decreased SV ➡️ decreased SBP ➡️ increased HR  + increased SVR due to catecholamine release leading to increased DBP  Obstructive“Obstruction of preload” ➡️ decreased SV➡️ low SBP ➡️ increased HR + increased SVR due to catecholamine release leading to increased DBPPneumothoraxIncreased intrathoracic pressure ➡️ decrease IVC and SVC ➡️ decreased preload Cardiac TamponadeFluid in pericardial space ➡️ decrease filling ➡️ decreased preloadPulmonary Emboli: Obstruction of RV to LA flow ➡️ decreased preload Wide Pulse Pressure: Distributive Shock “Warm shock”: Vasodilatation ➡️ decreased SVR ➡️ Decreased DBP Septic: Main cause of distributive shock Neurogenic: Loss of sympathetic tone ➡️ unopposed parasympathetic / vagal tone ➡️ decreased SVR ➡️ decreased DBP Anaphylaxis: histamine and other inflammatory mediators released ➡️ increased vascular permeability ➡️ decreased SVR ➡️ decreased DBP Adrenal Crisis: Not secreting cortisol ➡️ not increasing vascular tone ➡️ decreased SVR ➡️ decreased DBP  Hepatic Failure: Increase in NOS ➡️ increases NO ➡️ vasodilatation 🛌 Practical Bedside Approach When called to bedside:Is the patient meeting any of the 4 “L’s” ?Check the pulse pressure along with other vitalsWhy are they here? What’s the brief history?Narrow Pulse Pressure? Cardiogenic, hypovolemic, or obstructive shock Wide Pulse Pressure? Distributive shock Think: sepsis (most likely), neurogenic, anaphylaxis, adrenal crisis, hepatic failure 🚨 Clinical Bottom Line A brief but thorough bedside exam remembering the 4 “L’s”, a quick history, and examining the pulse pressure can help a clinician form a quick differential into the underlying etiology for a critically ill patient in shock. Stay sharp, stay systematic! 💡 Shock is a clinical diagnosis based on bedside findings — not just blood pressure readings.You don’t always need invasiv

🧭 REBEL Rundown 📌 Key Points 🩺 Sinus Tachycardia = Clinical Clue: Don’t just treat the number—it’s a sign of underlying physiologic stress.🧮 Oxygen Delivery Equation: HR ↑ may compensate for ↓ hemoglobin, O₂ sat, or cardiac output. Know: 👉 DO₂ = CO x Hb x Sat + 0.003(pO₂)🗂️ Systematic 8-Point Evaluation: 🫁 Airway/Hypoxia, 🌬️ Breathing , 💉 Circulation, 💊 Drugs,🩸 Erythrocytes (Anemia), 🌡️ Fever, 🍬 Glucose, 😖 “Holy Cow That Hurts”🧠 Think Holistically: Tachycardia isn’t the problem—what’s causing it is.🚫 Avoid Reflexive Beta Blockers: Don’t suppress a compensatory response before finding the cause.🔁 Reassess Frequently: Clinical status can change—stay vigilant. Click here for Direct Download of the Podcast. 📝 Introduction Sinus tachycardia is the most prevalent cardiac dysrhythmia in critically ill patients, yet it often receives less attention than it warrants. While the rhythm itself is not inherently dangerous, it serves as a crucial indicator of underlying physiological disturbances that require prompt evaluation and management. 🔑 Key Concepts Sinus Tachycardia as a Clinical Sign: Rather than focusing solely on the elevated heart rate, clinicians should interpret sinus tachycardia as a symptom pointing toward an underlying cause that needs to be identified and addressed.Oxygen Delivery Equation: Understanding the components of oxygen delivery—hemoglobin concentration, oxygen saturation, and cardiac output—is essential. An increase in heart rate may be a compensatory mechanism to maintain adequate oxygen delivery when other components are compromised. 8 Causes of Sinus Tachycardia Airway/Hypoxia: Ensure the airway is patent and assess for hypoxemia. Breathing: Evaluate for respiratory distress or pulmonary pathology.Circulation: Consider shock states, including hypovolemia, hemorrhage, or distributive shock. Drugs: Review medications and substances that may cause tachycardia, including stimulants and withdrawal states.Erythrocytes (Anemia): Assess for low hemoglobin levels that may impair oxygen delivery. Fever: Recognize that fever increases metabolic demand, leading to tachycardia.Glucose: Identify hypoglycemia or hyperglycemia as potential contributors.Holy Cow That Hurts: (Pain/Anxiety): Acknowledge that pain and emotional distress can elevate heart rate.  🛌 Practical Bedside Approach Holistic Assessment: Always interpret sinus tachycardia within the broader clinical context.Avoid Reflexive Treatment: Refrain from immediately administering rate-controlling medications without identifying and managing the underlying cause.Continuous Monitoring: Regularly reassess the patient’s status, as the underlying cause of tachycardia may evolve over time. 🚨 Clinical Bottom Line Sinus tachycardia is a vital clinical sign that necessitates a thorough and systematic evaluation to uncover and treat the root cause. By adopting this structured approach, clinicians can improve patient outcomes and avoid the pitfalls of symptomatic treatment without addressing underlying issues. Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO) 👤 Guest Contributors Eric Acker, MD Internal Medicine Resident, Rising Chief Resident, Cape Fear Valley Medical Center, Fayetteville NC Thirumala “Keerthi” Kammaripalle, MD Internal Medicine Resident, Rising Chief Resident Cape Fear Valley Medical Center, Fayetteville NC 🔎 Your Deep-Dive Starts Here It seems we can't find what you're looking for. The post REBEL Core Cast 137.0: A Simple Approach to Sinus Tachycardia appeared first on REBEL EM - Emergency Medicine Blog.

🧭 REBEL Rundown 📌 Key Points Short + shallow: Neuromuscular, bronchospasm, or compliance problem → act fast ⚠️Normal/large tidal volume: Compensation for metabolic/systemic causeUse all tools: 👁 Eyes: Chest rise, ✋ Hands: Palpate,👂 Ears: Listen, 🧠 Brain: Synthesize Click here for Direct Download of the Podcast. 📝 Introduction In this episode, we focus on the bedside evaluation of the tachypneic patient. Tachypnea (increased respiratory rate) can be an early indicator of serious illness, but not every tachypneic patient is on the verge of arrest. The key is honing your bedside assessment to recognize who is at risk for rapid deterioration and why. We break down a practical approach you can use immediately at the bedside. 🔑 Key Concepts First Priorities at the Bedside Chest Rise:Short, shallow respirations with poor chest rise are a major red flag.Patients with minimal tidal volumes are often approaching respiratory failure.Diaphoresis and Tachycardia:Diaphoresis + tachycardic patients with shallow breathing demand urgent attention as this is a sign of high catecholamine surge and impending respiratory collapse.Immediate Action:Use your eyes (chest rise), your ears (stethoscope), and brain (putting together all of the pieces together) Short, Shallow Breathing: Think Three Major Buckets Neuromuscular DiseaseMyasthenia gravis crisis, Guillain-Barré, myopathies, frailty.Weak inspiratory effort leads to low tidal volumes.Needs urgent positive pressure support (BiPAP, or intubation).Severe BronchospasmAsthma, COPD, anaphylaxis.Shallow, forced expirations signal airway obstruction.Silent Chest = airway emergency.Treat with bronchodilators, steroids, and positive pressure ventilation.Avoid immediate intubation if reversible; trial NIPPV first.Worsening Lung Compliance“Stiff lungs” harder to ventilate.Compliance (C) = Δ Volume / Δ PressureSo if it takes a lot of pressure to get adequate tidal volumes then your lungs are stiff and compliance is lowCauses include:Chest Wall: Rigidity, burn eschar.Pleural Space: Effusion, pneumothorax (check for asymmetric chest rise).Lung Parenchyma: Pneumonia, contusion, atelectasis.Below the Lung: Abdominal distension, ascites.Clinical pearl: Work outside-in (chest wall, pleura, lung, abdomen).  Normal to High Tidal Volumes with Tachypnea: Systemic Causes Metabolic Acidosis (e.g., DKA)Compensatory hyperventilation (Kussmaul breathing)Check a blood gas (VBG/ABG) to differentiate gap vs. non-gap acidosisRespiratory AlkalosisCauses: Pain, anxiety, fever, early sepsis, CNS issuesCentral drive increases respiratory rateAgain, ABG or VBG helps confirmDead Space VentilationPulmonary embolism (PE) is the classic cause.Other causes include:Severe emphysema: Alveolar walls are destroyed, so air reaches areas with no capillary blood flow.Pulmonary hypertension: High pressure damages and narrows vessels, reducing blood flow to ventilated alveoli.Low-flow states (shock): Poor systemic perfusion limits blood reaching alveoli, creating ventilated but under perfused areas.Excessive PEEP on ventilation: Overdistended alveoli compress nearby capillaries, blocking blood flow despite good ventilationKey concept: Easy to oxygenate, but tachypneic due to perfusion/ventilation mismatch.  🛌 Practical Bedside Approach Short, shallow breathing? Neuromuscular, bronchospasm, or compliance issueThink: Impending respiratory failure, act quickly.Normal to large tidal volumes? Systemic causesThink: Compensation (acidosis, pain, anxiety, PE).Use: Eyes (observe), Hands (palpate abdomen/chest), Ears (auscultate), Brain (synthesize). 🚨 Clinical Bottom Line A careful, simple bedside assessment can rapidly identify which tachypneic patients need immediate intervention—and help you avoid missing those headed toward respiratory collapse. Stay sharp, stay systematic! Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO) 👤 Guest Contributors Eric Acker, MD Internal Medicine Resident, Rising Chief Resident, Cape Fear Valley Medical Center, Fayetteville NC Micheal Bass DO Internal Medicine Resident, Rising Chief Resident Cape Fear Valley Medical Center, Fayetteville NC 🔎 Your Deep-Dive Starts Here REBEL Core Cast 123.0 – Posterior Epistaxis Take Home Points: Posterior epistaxis is a rare, life-threatning presentation. ... Head, Eye, Ear, Nose, and Throat Read More ANNEXA-1: Andexanet Alfa Associated with Harm in DOAC Reversal Background: In May of 2018, Andexanet alfa gained accelerated approval ... Hematology and Oncology Read More REBEL Core Cast 122.0 – Neutropenic Fever Take Home Points: There are many causes of neutropenia, chemotherapy ... Infectious Disease Read More REBEL Cast Ep126: Should We Not Be Recommending Small Adult BVMs in OHCA? Background: The holy grail of outcomes in OHCA is surv

🧭 REBEL Rundown 📌 Key Points 🫁 Hypoxemia = low blood oxygen🧠 Hypoxia = low tissue oxygen🔍 5 causes of hypoxemia, but most hospital cases are either:🚫 Shunt = doesn’t improve with oxygen therapy💨 Dead space = causes tachypnea but is easier to oxygenate💡 Always start with maximizing oxygen delivery (💊💨),but recognize quickly when positive pressure (🫁➡️) is needed️ V/Q mismatch🩸 Shunt (refractory to oxygen therapy) Click here for Direct Download of the Podcast. 📝 Introduction In this episode, we break down a practical bedside approach to hypoxemia. We clarify the difference between hypoxemia (low oxygen in the blood) and hypoxia (low oxygen at the tissue level), and walk through the major causes of hypoxemia that you need to recognize quickly at the bedside. 🔑 Key Concepts Hypoxemia vs. Hypoxia: Know the Difference Hypoxemia = Low oxygen in the blood.Measured indirectly by SpO₂ (pulse oximeter) or directly by PaO₂ (arterial oxygen tension) or SaO₂ (oxygen saturation).Hypoxia = Low oxygen at the tissue level.Can happen with or without hypoxemia. Four Types of Hypoxia Hypoxemic Hypoxia: Blood oxygen is low, so tissues get less oxygen. (e.g., severe pneumonia)Anemic Hypoxia: Low hemoglobin levels mean less oxygen-carrying capacity, even if oxygen levels are normal. (e.g., hemorrhage, hemolysis)Ischemic Hypoxia: Blood flow to tissues is blocked or reduced. (e.g., MI, stroke, severe shock)Histotoxic Hypoxia: Oxygen delivery is normal, but tissues can’t use it. (e.g., carbon monoxide or cyanide poisoning) Five Major Causes of Hypoxemia Hypopnea/Apnea (Decreased Respiratory Drive)Inadequate breaths (or no breaths) means lower oxygen intake.Seen in cardiac arrest, drug overdose, severe brain injury.Easy to recognize as patients are encephalopathic or apneic.High AltitudeLower barometric pressure = less available oxygen, despite 21% FiO₂.Rarely relevant inside hospitals, but important to know.Diffusion DefectImpaired oxygen transfer across alveoli, often due to chronic lung disease.Examples: interstitial lung disease, idiopathic pulmonary fibrosis.Patients are usually known to have underlying disease.V/Q Mismatch (Dead Space Disease)Problem with perfusion relative to ventilationCommon examples:Pulmonary embolism (classic dead space).Other causes include:Severe emphysema: Alveolar walls are destroyed, so air reaches areas with no capillary blood flow.Pulmonary hypertension: High pressure damages and narrows vessels, reducing blood flow to ventilated alveoli.Low-flow states (shock): Poor systemic perfusion limits blood reaching alveoli, creating ventilated but unperfused areas.Excessive PEEP on ventilation: Overdistended alveoli compress nearby capillaries, blocking blood flow despite good ventilation.Key concept: Easy to oxygenate, but tachypneic due to perfusion/ventilation mismatch.Key point: Patients often oxygenate “ok” at rest but are tachypneicShunt (Most Common and Most Concerning)“Crap in the alveoli” blocks oxygen diffusion:Pneumonia (pus)Pulmonary edema (water)Atelectasis (collapse)Pulmonary hemorrhage (blood)Blood moves from right to left without being oxygenated.Refractory hypoxemia despite oxygen therapy = shunt physiology.Key Move: High FiO₂ (non-rebreather mask) → if still hypoxemic, they need positive pressure (NIV or intubation). 🛌 Practical Bedside Approach Give as much FiO₂ as possible (non-rebreather mask).Watch SpO₂ response:If it improves → V/Q mismatch or dead space more likely.If it doesn’t improve → think shunt physiology.If refractory hypoxemia persists → Start positive pressure ventilation (HFNC, CPAP, BiPAP, or intubation depending on the situation). 🚨 Clinical Bottom Line Mastering the basics of hypoxemia helps you recognize dangerous physiology early — before your patient crashes. Keep in mind the four types of hypoxia and the five major causes of hypoxemia. Post Peer Reviewed By: Marco Propersi, DO (Twitter/X: @Marco_propersi), and Mark Ramzy, DO (X: @MRamzyDO) 👤 Guest Contributor Eric Acker MD Internal Medicine Resident, Rising Chief Resident, Cape Fear Valley Medical Center, Fayetteville NC Meet The Team 🔎 Your Deep-Dive Starts Here REBEL Cast – EMTALA + Reproductive Health Rights REBEL Cast – EMTALA + Reproductive Health Click here for ... Ethical and Legal Read More REBEL Cast Ep125: 1st 48 Hours of PE Management – How Good Is Unfractionated Heparin? Background: The mainstay of treatment for symptomatic pulmonary embolism  (PE) ... Cardiovascular Read More REBEL Cast Ep124: Nitrates in Right Sided MIs? Background: Nitrates can help improve symptoms and ischemia in the ... Cardiovascular Read More REBEL Core Cast 118.0 – IM vs PO NSAIDs REBEL Core Cast 118.0 – IM v

Acetaminophen (APAP) overdose remains one of the most common causes of acute liver failure in the United States. While its therapeutic use is widespread and generally safe, unintentional overdoses and delayed presentations can lead to devastating outcomes. In this episode of REBEL Cast, we break down the pathophysiology, clinical course, diagnostic approach, and evidence-based management of APAP toxicity—including when to initiate NAC, how to apply the Rumack-Matthew nomogram, and the evolving role of adjunctive therapies like fomepizole. Whether you’re in the ED or elsewhere , this is core content every clinician should know. Click here for Direct Download of the Podcast. Definition and Physiology After ingestion of a therapeutic dose, immediate release APAP is absorbed with a time to peak concentration anywhere between 30-45 minutes. In the context of extended-release, formulations, full absorption is typically reached by 4 hours post-ingestion.1 In therapeutic dosing, the vast majority of APAP undergoes hepatic conjugation with glucuronide or sulfate to form benign metabolites that ultimately get excreted in the urine. The remaining ~5% is oxidized by CYP2E1 to form N-acetyl-p-benzoquinoeimine (NAPQI). NAPQI is hepatotoxic. Glutathione combines with NAPQI to generate non-toxic metabolites that are also eliminated in the urine. In overdose, the amount of NAPQI that is generated is increased as the typical metabolic pathways become saturated. The NAPQI that remains leads to hepatocellular death in Zone 3 of the liver (or the centrilobular location) which is the area with the largest degree of oxidative metabolism. Clinical Manifestations and Diagnostic Evaluation The clinical course of acute APAP toxicity is classically broken into four different stages. Stage1: this is generally within 24 hours. Patients are either asymptomatic or have non-specific GI symptoms (nausea, vomiting, malaise). At this point, hepatic function testing is normal. Stage2: ~24-72 hours. The onset of hepatic injury marks this stage. Aspartate aminotransferase (AST) is the most sensitive marker to detect hepatic dysfunction; AST elevated is nearly universal by 36 hours post-ingestion. Stage3: defined as peak hepatotoxicity; generally between 72-96 hours post-ingestion. Patients may manifest hepatic encephalopathy or coma. AST and/or ALT might rise above 10,000 IU/L. Other lab abnormalities include: INR/PT, glucose, lactate, pH, and creatinine. Death from fulminant hepatic failure usually occurs anywhere between 3-5 days after an acute ingestion. Mortality is often secondary to multiorgan failure, ARDS, sepsis, or cerebral edema. Stage4: often called the “recovery phase.” Patient who survive demonstrate complete hepatic generation without any evidence of hepatic dysfunction. The following labs should be obtained for severe APAP ingestions: APAP Concentration, hepatic panel, pH, coagulation panel, renal function, lactate and phosphate. These labs will ultimately dictate disposition (see King’s College Criteria below) Management Consider GI decontamination with activated charcoal as this can reduce systemic absorption and limit subsequent clinical sequalae. Ingestions should be classified as acute or repeated supratherapeutic (“chronic” ingestions) Single Acute Ingestion If feasible, obtain a 4 hour post-ingestion APAP concentration. Any concentration earlier than 4 hours is uninterpretable as subsequent concentrations may increase or decrease depending on the clinical scenario. Concentrations between 4-8 hour post-ingestion can be plotted on the Rumack-Matthew nomogram to determine when NAC should be initiated. If the APAP concentration is above the plotted line, NAC should be started. NAC is nearly 100% effective if started within 8 hours post-ingestion.2 If an APAP concentration is unable to be drawn before 8 hours or if LFTs are already elevated, NAC should be empirically started if the pre-test probability is high enough for clinical concern. Repeated Supratherapeutic/Chronic Ingestions Cannot apply the Rumack-Matthew Nomogram If LFTs are elevated or if there is a positive APAP concentration, NAC should generally be started however consultation with a toxicologist or Poison Control Center is advised as these cases are often complicated. N-Acetyl-Cysteine (NAC) Dosing “3 Bag Protocol” – 21 hour regimen 150mg/kg over 1 hour loading dose 50mg/kg over 4 hours = 12.5 mg/kg/hr 100mg/kg over 16 hours = 6.25 mg/kg/hr Risk: anaphylactoid reaction Reaction is rate related and typically occurs during the loading dose Symptoms: flushing, urticaria. NAC should be continued until all of the following criteria are met: Negative APAP concentration “Significant Decreased in AST”: defined as either <1000 IU/L or a 25-50% drop from the peak. No evidence of hepatic failure If criteria are not met, the third bag should be extended indefinitely. The King’s Colle

Introduction: In this episode of Rebel Cast, host Marco Propersi, along with co-hosts Steve Hochman and Kim Baldino, delve into the practice and importance of street medicine—the direct delivery of healthcare to homeless and unsheltered individuals. Special guests Dr. Jim O’Connell, a pioneer of street medicine, and Dr. Ed Egan, a recent street medicine fellowship graduate, share their experiences and insights on serving this vulnerable population. They discuss the origins, scope, and challenges of street medicine, the ethical dilemmas faced, and the profound impact of building trust and community with patients. The conversation underscores the necessity of integrating street medicine with mainstream healthcare systems and emphasizes that small acts of kindness and persistence can significantly improve the lives of those experiencing homelessness. REBEL Cast – Street Medicine: Compassionate Care for the Unhoused Click here for Direct Download of the Podcast. 00:00 Introduction to Rebel Cast 00:18 Meet the Hosts and Guests 00:47 Understanding Street Medicine 02:22 Origins and Early Challenges 07:23 Street Medicine in Practice 20:11 Barriers to Care 22:23 Housing First Experiment 26:56 Ethical Dilemmas in Street Medicine 27:52 Challenges of Providing Care on the Streets 29:56 The Role of Street Medicine Teams 31:17 The Importance of Building Trust 33:55 Limitations and Realities of Street Medicine 37:37 The Future of Street Medicine 41:42 Integrating Street Medicine with Emergency Medicine 43:36 Personal Reflections and Lessons Learned 48:56 Advice for Aspiring Street Medicine Practitioners 53:03 Final Thoughts and Encouragement Links: Street Medicine Institute National Healthcare for the Homeless Council EMRA Fellowship Guide: Opportunities for Emergency Physicians, 3rd ed. The post Street Medicine: Compassionate Care for the Unhoused appeared first on REBEL EM - Emergency Medicine Blog.

Take Home points: Always suspect an open joint if there is a laceration, regardless of size, the lies over joint CT scan of the affected joint is widely considered to be the standard approach to evaluation but the saline load test may be useful in certain circumstances. Obtain emergency orthopedics consultation for all open joints and administer antibiotics and update tetanus in all patients   REBEL Core Cast 131.0 – Traumatic Arthrotomy Click here for Direct Download of the Podcast. Definition: a deep laceration that extends into the joint capsule, exposing the intra-articular surface to the environment A laceration into the joint exposes the normally sterile intra-articular contents to external contamination Inoculation of the joint often results in septic arthritis Physical Exam: Laceration over joint (can be variable in size) Local wound exploration may be sufficient in identifying the open joint Exam findings suspicious for joint capsule involvement: Air bubbles Extravasation of joint fluid – straw colored, viscous, sometimes oily in appearance Diagnostic testing: Imaging: X-ray Limited ability to see air in joints but a reasonable first test CT scan Intra-articular air visualized on CT (Konda 2013) May be up to 100% sensitive for joint violation Study limited by small numbers, inclusion bias + inadequate gold standard May be considered the standard evaluation modality in many settings. Saline load test Has mainly been supplanted by CT scan due to ease in obtaining, reported performance characteristics, consultant recommendation and difficulty in interpreting test. Useful if physical examination equivocal or plain radiographs non-diagnostic Technique (Video) Perform arthrocentesis of the joint with a large bore needle (18-20 gauge) Sterile saline is injected into the joint while passive movement is applied to the joint The laceration site is watched for saline extravasation indicating communication between the joint and external environment Sensitivity ranges from 34%-99% depending on the study, joint, and the amount of saline used to load the joint (Browning 2016) Methylene blue Aids in distinguishing a true positive from additional bleeding from the wound Recent studies suggest that the addition of methylene blue does not increase sensitivity if a sufficient amount of saline is used (Metzger 2012) Volume of fluid injected Varies depending on the joint in which you are injecting Higher volumes increase sensitivity but also increase pain for the patient Knee Joint (Keese 2007) 50 ml: Sensitivity of about 46% 194 ml: sensitivity of 95% Elbow Joint (Feathers 2011) 20 ml: Sensitivity of 86% 40 ml: Sensitivity of 95% Ankle Joint (Bariteau 2013) 7 ml: Sensitivity of 50% 30 ml: Sensitivity of 95% ED Management: Reduce open fractures if present Irrigate grossly contaminated wounds in the ED Immobilize the joint to prevent further injury Obtain early orthopedic evaluation for joint exploration, and washout to be performed within 6-24 hours Tetanus prophylaxis Prophylactic antibiotics (best if given within 6 hours) Staph/strep coverage: 1st generation cephalosporin (i.e. cefazolin or cefuroxime) If risk factors for MRSA present, use agent with activity against MRSA (i.e. vancomycin) If significant soft tissue injury, add gram negative coverage like late generation cephalosporin, extended-spectrum penicillin, or aminoglycoside (i.e. gentamycin) If concern for fecal or clostridial infection, add high dose penicillin (i.e. zosyn) If seawater contamination and concern for vibrio vulnificus, add doxycycline Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie) The post REBEL Core Cast 131.0 – Traumatic Arthrotomy appeared first on REBEL EM - Emergency Medicine Blog.

Take Home Points Early diagnosis: erythema and warmth of the skin surrounding the umbilicus isn’t normal. Get labs, start abx and get the patient admitted Consult peds surgery on all of these patients as progression to nec fast, while uncommon, is devastating If the patient appears toxic or has systemic symptoms, the simply omphalitis has progressed and aggressive treatment including surgery is likely indicated REBEL Core Cast 130.0 – Omphalitis Click here for Direct Download of the Podcast. Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie) The post REBEL Core Cast 130.0 – Omphalitis appeared first on REBEL EM - Emergency Medicine Blog.

Take Home Points Orogastric lavage may still play an important role in treatment of the overdose patient.  Do not perform lavage if the ingestion has limited toxicity at any dose or the ingested dose is unlikely to cause significant toxicity. Strongly consider orogastric lavage in a patient who has taken an overdose of drugs that are particularly toxic, suspected extreme doses associated with high morbidity/mortality and do not have easily available and effective antidotes. Secure the airway prior to placing the lavage tube to minimize aspiration risk. REBEL Core Cast 129.0 – Gastric Lavage Click here for Direct Download of the Podcast. Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie) The post REBEL Core Cast 129.0 – Gastric Lavage appeared first on REBEL EM - Emergency Medicine Blog.

Take Home Points Toxic alcohols generally refer to methanol and ethylene glycol as these substances pose significant metabolic derangement and end-organ damage. Patient who present shortly after ingestion will simply look inebriated – no different than ethanol intoxication. At this point, patients will have an elevated osmolar gap and little to no anion gap. Patient who presents in a delayed fashion after ingestion may have a normal osmolar gap however will manifest the signs of end-organ damage: anion gap metabolic acidosis, visual impairment, or renal dysfunction. The osmolar gap is poorly sensitive, specific surrogate measure that is used to detect the presence of toxic alcohols. A normal osm gap does not rule out a toxic alcohol ingestion. Management includes fomepizole, hemodialysis, and vitamin supplementation.   REBEL Core Cast 128.0 – Toxic Alcohols Click here for Direct Download of the Podcast. Reference: Wiener SW. Chapter 106. Toxic Alcohols. In: Nelson LS, Howland MA, Lewin NA, Smith SW, Goldfrank LR, Hoffman RS, , Flomenbaum NE. eds. Goldfrank’s Toxicologic Emergencies, 11e New York, NY: McGraw-Hill; 2019. Accessed October 2, 2024. Guest Expert: Dr. Sanjay Mohan, MD (Link) Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie) The post REBEL Core Cast 128.0 – Toxic Alcohols appeared first on REBEL EM - Emergency Medicine Blog.

Take Home Points Anticipate anatomically challenging airways and consider early intubation prior to loss of airway anatomy. Skip the zones of the neck and focus on hard signs of vascular (Shock w/o another source, Pulsatile bleeding, Expanding hematoma, Audible bruit, Signs of stroke) or aerodigestive (Airway compromise, Bubbling wound, Extensive SubQ air, Stridor, Significant hemoptysis/hematemesis). The presence of hard signs indicates the need to go to the OR or for angiographic intervention. Control hemorrhage with a single finger and direct pressure. REBEL Core Cast 127.0 – Penetrating Neck Injuries Click here for Direct Download of the Podcast. Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie) The post REBEL Core Cast 127.0 – Penetrating Neck Injuries appeared first on REBEL EM - Emergency Medicine Blog.

Background: Cath lab activation based on ST-elevation myocardial infarction (STEMI) criteria is founded on aging data and requires evolution. In the “Occlusive Myocardial Infarction (OMI) Manifesto,” emergency physicians Dr. Steve Smith, Dr. Pendell Meyers, and Dr. Scott Weingart introduced a new paradigm —OMI vs. non-occlusive myocardial infarction (NOMI). The OMI/NOMI paradigm focuses on the presence of coronary occlusion, while STEMI/NSTEMI categorizes myocardial infarctions based on electrocardiogram (ECG) findings. Patients with OMI exhibit higher mortality and worse left ventricular function compared to those with NOMI.1, 2, 3 Detecting OMI is more difficult and necessitates scrutiny of the ECG, which is challenging in a busy emergency department where ED clinicians are interrupted more than ten times per hour.4, 5 Some OMI ECG signs include ST elevation in only one lead, subtle ST elevation with minimal reciprocal changes, isolated ST depressions, and hyperacute T waves. To meet this challenge, Dr. Steve Smith, Dr. Pendell Meyers (Dr. Smith’s ECG Blog), and their team developed The Queen of Hearts, a machine-learning AI model that has the potential to aid in the early detection of subtle OMI ECG changes. Accurately identifying OMI changes in ECG that STEMI criteria might otherwise miss would allow for more timely intervention, potentially salvaging more myocardium. An AI model that is highly sensitive in detecting OMI while maintaining a high degree of specificity would be an ideal tool to support emergency physicians’ clinical decision-making. The performance of this tool is unknown. Click here for Direct Download of the Podcast. Paper: Herman R, Meyers HP, Smith SW, et al. International evaluation of an artificial intelligence-powered electrocardiogram model detecting acute coronary occlusion myocardial infarction. Eur Heart J Digit Health. 2023;5(2):123-133. Published 2023 Nov 28. PMID: 38505483 Clinical question: “Can an AI model detect an OMI lesion using a single 12-lead ECG?” What They Did: Investigators performed a retrospective derivation study followed by validation on an internal data set from the same Acute Coronary Syndrome (ACS) database. Cases eligible for inclusion were randomly assigned to a model development training set (derivation set) and testing set (validation set).   The training set included ECG feature extraction and classification Feature extraction used 60,000 parameters The classification component combined all extracted features and used an additional 150,000 parameters. The validation data set was used for hyperparameter tuning and threshold selection.  Investigators then tested the AI model on two data sets An internal European data set (internal validation set) A separate US data set (external validation set) from the DOMI ARIGATO database. They compared the AI model with the existing criteria for detecting OMI on 12-lead ECGs and analyzed the AI model in various subgroups. Population: Derivation Set: Random selection of ACS patients from the Cardiovascular Centre Aalst in Belgium and ACS patients from an international image database patient. EU Internal Test Set: Random Selection of ACS patients from the Cardiovascular Centre Aalst in Belgium and ACS patients from an international image database patient. US External Test Set: Patients from the DOMI ARIGATO database. Exclusion: ECGs >24 h before CAG and post-CAG ECGs with poor signal quality  ECGs with missing Expert Annotation, undigitizable ECGs, Baseline ECGs (additionally excluded from the US External Database) Intervention: AI-powered ECG model implemented on ECGs from the internal EU and external US datasets. Comparator: Blinded physician annotations of the standard ‘STEMI criteria’ on ECG Blinded subjective ECG expert annotations of OMI Angiographic clinical outcome data Outcomes: Primary Outcome: AI model’s ability to identify patients with angiographically confirmed OMI using only the 12-lead ECG. Secondary Outcomes: OMI AI model performance across demographic and ECG subgroups A comparison of the AI model performance against the existing STEMI criteria for detecting acute coronary occlusion from 12-lead ECGs A sensitivity analysis of AI model performance using various angiographic and laboratory cut-offs of OMI An evaluation of misclassified cases Results: The derivation set used in the AI model development included 18,616 ECGs from 10,543 patients with clinically validated outcomes. The overall test set included 3254 ECGs from 2222 patients   The internal EU testing cohort 2016 ECGs from 1630 patients  The US testing cohort 1238 ECGs from 633 patients  The prevalence of OMI differed between the internal EU and the external US test sets, 16% compared with 36.2%, respectively ( < 0.001). The patients in the US test set were younger, had more ECGs recorded before catheterization, and were more lik

Take Home Points Early administration of antibiotics (within 60 min) in patients with fever and neutropenia is life saving. Fever in sickle cell is an emergency and always requires cultures and antibiotics even if the child appears well. Avoid sedation and lying supine and steroids in patients with mediastinal masses. Red flags in patients with headaches that may suggest a brain tumor  include signs of increased intracranial pressure, focal neurological signs, seizures or ataxia. REBEL Core Cast 126.0 – Peds Hem Onc Emergencies Click here for Direct Download of the Podcast. Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie) The post REBEL Core Cast 126.0 – Peds Hem Onc Emergencies appeared first on REBEL EM - Emergency Medicine Blog.

Take Home Points Always obtain an EKG in patients with ESRD upon presentation Always obtain an EKG in patients with hyperkalemia as pseudohyperkalemia is the number one cause If the patient with hyperkalemia is unstable or has significant EKG changes (wide QRS, sine wave) rapidly administer calcium salts In patients who are anuric, early mobilization of dialysis resources is critical REBEL Core Cast 125.0 – Hyperkalemia Click here for Direct Download of the Podcast. Definition: A serum potassium level > 5.5 mmol/L Epidemiology Common electrolyte disorder 10% of hospitalized patients (Elliott 2010) Causes Pseudohyperkalemia: extravascular hemolysis Renal failure (potassium is primarily eliminated by the kidneys) Acidosis Massive cell death (tumor lysis syndrome, rhabdomyolysis, burns, crush injuries, hemolysis) Drugs: ACEI, ARBs, Spironalactone, NSAIDs, Succinycholine Clinical Manifestations Mild hyperkalemia often asymptomatic Cardiac Effects Increased potassium raises the resting membrane potential of cardiac myocytes Slows ventricular conduction Decreases length of action potential Increases cardiac myocyte excitability Cardiac effects can manifest in lethal dysrhythmias Neuromuscular Effects Paresthesias Weakness Flaccid paralysis Depressed or absent deep tendon reflexes Diagnosis Suspect hyperkalemia in ALL patients with renal impairment, especially end-stage renal disease (ESRD) Serum potassium Can be artificially elevated by extravascular hemolysis Blood gas results may differ from standard metabolic panels by up to 0.5mmol/L 12-Lead EKG Screening test that can rapidly detect severe cardiac manifestations of hyperkalemia A normal EKG with a significant serum potassium elevation should raise concerns for spurious results (extravascular hemolysis) Sensitivity of EKG to detect hyperkalemia is poor (Wrenn 1991, Aslam 2002, Montague 2008) Classic EKG findings PR prolongation Peaked T waves Loss of P waves Widening of QRS complex Sine wave Ventricular Fibrillation Asystole Note: Hyperkalemia can present with a number of “non-classic” EKG findings including AV blocks and sinus bradycardia (Mattu 2000) Note: Hyperkalemic EKG changes do not necessarily occur in order (i.e. patients can jump from peaked T waves to sine wave) Management Basics: ABCs, IV, O2, Cardiac Monitor and, 12-lead EKG Identify + treat underlying cause of hyperkalemia (i.e. rhabdomyolysis -> hydration) Remove inciting factors (i.e. stop ACEI, NSAIDs etc) Asymptomatic Patients without EKG Changes Eliminate potassium from the body Binding agents (SPS, Sodium zirconium cyclosilicate etc) Enhance renal elimination Intravenous hydration if volume depleted Consider potassium wasting loop diuretics (i.e. furosemide) Dialysis for anuric patients (i.e. ESRD) Symptomatic Patients or Significant EKG Changes Stabilize cardiac myocytes with calcium salts Mechanism: Recreates the electrical gradient leading to rapid reversal of cardiac effects and rapid stabilization Two Options: CaGluconate, CaCl2 No difference in time to onset (1st pass metabolism is a myth) Dose: 1 ampule CaCl2 (270 mg Ca2+) = 3 ampules CaGluconate (90 mg Ca2+/ampule) Onset of action: seconds to minutes Duration: 20-30 minutes Shift potassium into intracellular space (temporary) Insulin (Moussavi 2021) Mechanism: Activation of the Na-K-ATPase Dose: 5-10 units IV Onset of Action: < 15 min Effect: Lowers potassium by about 0.6 mmol Duration of action: 30-60 min Give with dextrose (0.5 – 1 g/kg) unless hyperglycemia present Caution: Duration of action of insulin may outlast administered dextrose. Be vigilant for hypoglycemia Beta-adrenoreceptor agonists (i.e. albuterol) Mechanism: Activation of beta receptors Dose: 10-20 mg inhaled (4-8 standard ampules) Onset of Action: < 15 min Effect: Lowers potassium by about 0.6 mmol Duration of action: 30-60 min Additive effect with insulin (Allon 1990) Note: Unlikely to have effect in patients taking beta-adrenoreceptor blocker medications Sodium Bicarbonate (NaHCO3) Evidence for the efficacy of NaHCO3 to lower serum potassium is scant and contradictory (Elliott 2010, Weisberg 2008) Eliminate potassium from the body (see above) Asymptomatic Patients with Minor EKG Changes Minimal recommendations on managing this clinical entity Eliminate potassium from the body (see above) Consider calcium salt administration: patients can rapidly progress through EKG changes and calcium administration may prevent this from occurring. However, the effects of calcium are temporary and offer no long-term protection Consider medications to shift potassium intracellularly while waiting for elimination Take Home Points Always obtain an EKG in patients with ESRD upon presentation Always obtain an EKG in patients with hyperkalemia as pseudohyperkalemia is the number one cause If the patient with hyperkalemia is unstable or has significant EKG changes (wide QRS, sine wave) rapidly administer calcium salts In patients who are anuric,

Take Home Points Management of severe beta-blocker and calcium-channel blocker toxicity should occur in a stepwise fashion: potential gastric decontamination, multiple lines of access, judicious fluids, calcium, glucagon, and vasopressors as needed. Initiation of high dose insulin therapy requires a tremendous amount of logistical and cognitive resources as it requires cross-disciplinary collaboration and is prone to mismanagement. If the patient doesn’t respond to maximum pharmacologic therapy, venous-arterial ECMO should be considered. REBEL Core Cast 124.0 – Hyperinsulinemia Euglycemia Therapy Click here for Direct Download of the Podcast. Background and Physiology Shock secondary to beta-blocker (BB) or calcium-channel blocker (CCB) toxicity bears a tremendous degree of morbidity and mortality. According to the 2022 Annual Report of the National Poison Data System from America’s Poison Center, CCBs and BBs account for the sixth and seventh largest number of fatalities from overdose.1 Recall that cardiac output is a function of both stroke volume and heart rate. The natural response to diminishing stroke volume is a compensatory rise in heart rate (tachycardia). Keep a low threshold to search a patient’s medication list for BB/CCBs, when a hypotension is seen with a “normal heart rate.” Clinical Manifestations Both BBs and CCBs ultimately cause reduced levels of intracellular calcium within myocytes. Depending on the degree of toxicity, subsequent effects include: decreased systemic vascular resistance, vasodilation, bradycardia, various conduction delays, and ultimately hypotension and cardiogenic shock. In addition to abnormal vital signs, look for surrogates of poor clinical perfusion: acidemia, lactate, decreasing urinary output Traditional Management Consider GI decontamination to reduce systemic absorption: 1g/kg up to 50g of activated charcoal. Patient must be alert or the airway must be secured as to avoid aspiration. Obtain multiple lines of intravenous access (3 PIVs or triple lumen CVC) and provide a judicious amount of fluids. (more on this below) Pharmacotherapy Calcium Gluconate: 1-3g intravenous Glucagon: 3mg-5mg slow intravenous push. Rapid administration may induce nausea and emesis. Vasopressors as a bridge to… HIET Mechanism of action is still not fully elucidated however several factors are implicated: Insulin augments cardiac contractility by activating “reverse-mode” Na-Ca exchange and subsequently increasing calcium concentration in the sarcoplasmic reticulum. 2 At a resting physiologic state, the heart utilize free fatty acids as its primary energy course. Under stressed conditions, glucose is used instead. Insulin helps to facilitate glucose metabolism. HIET Dosing: 1 unit/kg IV bolus. Then infusion starting at 1 unit/kg/hr infusion and titrate q30-60 minutes, keeping in mind that effects are not instant. Relative maximum is ~10 unit/kg/hr. If glucose <250 mg/dL, administer a bolus of dextrose 25-50 g (or 0.5-1 g/kg) IV. Ask pharmacy to concentrate insulin from 1 unit/mL to 10 units/ml. Patients often succumb to volume overload given pre-existing cardiac disease and the volume of medical resuscitation through their hospital stay. Once HIET is initiated, dextrose and potassium infusions should simultaneously be started to obviate hypoglycemia and hypokalemia Dextrose: 0.5-1 g/kg/hr via D50/D20 Replete potassium to a minimum of 3.5mEq/L A central venous catheter (often a triple lumen) is often needed to emergently replete potassium and provide D50/D20 safely (given its high osmolarity) Serial monitoring of dextrose (q15-30 minutes) and potassium (q1 hour) is critical HIET has been demonstrated to improve perfusion without necessarily increasing SVR/MAP – while MAPs may not markedly increase dramatically in the short term, obtain serial blood gases, lactate, and track urinary output to track perfusion. 3 Hyperinsulinemia Euglycemia Therapy (HIET) for BB/CCB Toxicity Management of severe beta-blocker and calcium-channel blocker toxicity should occur in a stepwise fashion: potential gastric decontamination, multiple lines of access, judicious fluids, calcium, glucagon, and vasopressors as needed. Initiation of high dose insulin therapy requires a tremendous amount of logistical and cognitive resources as it requires cross-disciplinary collaboration and is prone to mismanagement. HIET Dosing: 1 unit/kg IV bolus. Then infusion starting at 1 unit/kg/hr infusion and titrate q30-60 minutes, keeping in mind that effects are not instant. Relative maximum is ~10 unit/kg/hr. HIET therapy requires simultaneous dextrose and potassium infusions as insulin will induce hypoglycemia and shift potassium intracellularly. If the patient doesn’t respond to maximum pharmacologic therapy, venous-arterial ECMO should be considered. References Gummin DD, Mowry JB, Beuhler MC, et al. 2022 Annual Report of the National Poison Data

Take Home Points: Posterior epistaxis is a rare, life-threatning presentation. The key is in identifying and rapidly gaining control with a posterior pack or foley catheter. These patients often require surgical intervention so get ENT to the bedside and admit to a place with a higher level of monitoring. REBEL Core Cast 123.0 – Posterior Epistaxis Click here for Direct Download of the Podcast. Recognition Typically will have heavy bleeding both anteriorly and posterior into the oropharynx. These patients have a tough time because they’re continually trying to spit out or swallow blood Tachycardia is common and hypotension while not common isn’t unexpected. Very different from anterior epistaxis where VS usually unremarkable or maybe a bit of hypertension Failure of anterior pressure or packing to stop bleeding: apply pressure but still see brisk posterior bleeding or even place b/l pack and see continued posterior bleeding Start with the basics IV, Supp O2, Monitor Consider blood products if the patient appears to be losing a lot of blood or they report heavy blood loss. VS abnormalities can drive this as well Strongly consider reversal of AC (this will typically come after control) Stopping the Bleeding PPE: these things bleed like stink. Anecdote. Gown, gloves and most importantly eye and face protection Ideal: commercial posterior pack Two balloons – one for anterior, one for posterior Place the device (straight back parallel to the floor) Inflate anterior balloon (10-15 cc) of air If still bleeding, inflate posterior balloon (5-10 cc of air) Foley: if no commercial device Place foley catheter just as you would place a nasal tampon When you see the tip of the foley in the posterior pharynx, inflate balloon (5-10 cc) Need to pull back a bit and secure (can do this with tape on the nose) Post Placement Care Antibiotics: standard practice to give cephalexin or amox/clav. Literature doesn’t defend this approach but, the lit is pretty sparse. The idea behind abx is to prevent things like AOM and TSS but neither should be much of an issue with short term placement ICU Admission? Traditional teaching is that these patients are at risk for life-threatening bradydysrhythmias and should go to the ICU Literature here is non-existent. Two oft-cited articles Cassisi Laryngoscope 1971 – no mention of cardiac events in the article but widely cited Zeyyan Laryngoscope 2010 – slightly lower HR in the packing group but no bradydysrhythmias Before throwing ICU out Hypoxia can occur – Cassisi found about a 20 mm Hg drop in PaO2 but all the patients in this publication were sedated so the packing may not have been the issue look at Viducich 1995 Acad Emerg Med – showed that 18% of the 88 patients with posterior epistaxis required a surgical intervention. With that in mind, you want to consider placing patients into a setting where they can be frequently reassessed – perhaps SDU. This will be pretty location specific. If you treat a posterior bleed at a hospital without ENT, I would transfer as surgical intervention is pretty common REBEL EM: Do Patients with Epistaxis Managed by Nasal Packing Require Prophylactic Antibiotics? REBEL EM: Do Patients with Posterior Epistaxis Managed by Posterior Packs Require ICU Admission? EMRAP HD: Epistaxis Posterior Pack References Cassisi NJ et al. Changes in arterial oxygen tension and pulmonary mechanics with the use of posterior packing in epistaxis: a preliminary report. Laryngoscope 1971; 81(8): 1261-6. PMID: 5569677 Zeyyan E et al. The effects on cardiac function and arterial blood gas of totally occluding nasal packs and nasal packs with airway. Laryngoscope 2010; 120: 2325-2330. PMID: 20938948 Loftus BC et al. Epistaxis, medical history and the nasopulmonary reflex: what is clinically relevant. Otolaryngol Head Neck Surg 1994; 110: 363-9. PMID: 8170679 Viducich RA et al. Posterior epistaxis: clinical features and acute complications. Acad Emerg Med 1995; 25(5): 592-6. PMID: 7741333 Corrales CE, Goode RL. Should patients with posterior nasal packing require ICU admission. Laryngoscope 2013; 123: 2928-9. PMID: 24114977 Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie) The post REBEL Core Cast 123.0 – Posterior Epistaxis appeared first on REBEL EM - Emergency Medicine Blog.

Background: In May of 2018, Andexanet alfa gained accelerated approval by the FDA for the reversal direct oral anticoagulants (DOACs) despite a lack of robust evidence for use. The 2022 AHA/ASA guidelines give the drug a level 2A recommendation and recommend it over the use of 4F-PCC (Greenberg 2022). FDA approval alongside guideline endorsement has led to the drug seeing a remarkable growth in use without a single high-quality study to support its use. The available data reports good hemostatic control: a subjective measure that is highly biased by unblinding and selection bias. More importantly, there are no studies comparing andexanet alfa to 4F-PCC or even placebo looking at important, patient-centered outcomes. REBEL Cast WEE – ANNEXA-1 – Andexanet Alfa Associated with Harm in DOAC Reversal Click here for Direct Download of the Podcast. Article: Connolly SJ et al. Andexanet for Factor Xa Inhibitor-Associated Acute Intracerebral Hemorrhage (ANNEXA-1). NEJM 2024; 390(19): 1745-55. PMID: 38749032 Clinical Question: Does the use of andexanet alfa in patients on DOACs with intracerebral hemorrhage improved hemostatic efficacy? Population: Patients > 18 years of age on a factor Xa inhibitor (taken within 15 hours of randomization) with an acute intracerebral hemorrhage. Outcomes: Primary: Hemostatic efficacy assessed at 12 hours after randomization. Hemostatic efficacy was defined as: Excellent hemostatic efficacy: Change in hematoma volume < 20% Good hemostatic efficacy: Change in hematoma volume < 35% Increase in NIHSS < 7 points at 12 hours No receipt of rescue therapies within 3-12 hours from randomization No surgery to decompress the hematoma within 3-12 hours from randomization. Secondary: Percent change from baseline in anti-factor Xa activity during the first 2 hours from randomization Safety Endpoints (assessed at 30 days) Thrombotic events (ischemic stroke, myocardial infarction, VTE). Death Intervention: Andexanet alfa high-dose or low-dose bolus followed by infusion depending on time and dose from last DOAC use. Control: Usual care Design: Non-blinded, randomized controlled trial performed at 131 centers across 23 countries over 4 years. Exclusions GCS < 7 at the time of consent NIHSS > 35 Surgery planned within 12 hours of enrollment Thrombotic event within 2 weeks of enrollment Time from symptom onset > 6 hours Pregnancy Results: Primary results 581 patients were assessed for eligibility across 131 sites over 4 years 31 excluded prior to randomization 20 excluded after randomization due to consent issues 530 analyzed for the safety outcomes 263 patients assigned to andexanet alfa arm 267 patients assigned to usual care arm 452 patients were analyzed for the primary outcome 85.5% (195/228) patients in the usual care arm received 4F-PCC 78.1% (175/224) patients in the andexanet arm received the low-dose regimen Critical Results Andexanet alfa Usual Care Difference (95% CI) P Value Primary Outcome Hemostatic Efficacy 67% (150/224) 53.1% (121/228) 13.4 (4.6 – 22.2) 0.003 NIHSS change < 7 points 87.9% (188/214) 83.0% (181/218) 4.6 (-2.0 – 11.2) Secondary Outcome Anti-Factor Xa % Change -94.5% (-96.6 – 88.9) -26.9% (-54.2 – -9.5) Safety Outcome Thrombotic Events 10.3% 5.6% 4.6 (0.1 – 9.2) 0.048 TIA 0 0 Ischemic Stroke 6.5% 1.5% Myocardial Infarction 4.2% 1.5% DVT 0.4% 0.7% PE 0.4% 2.2% Arterial Embolism 1.1% 0.7% Death 27.8% 25.5% 0.51 Strengths: This is the first randomized trial comparing andexanet alfa to standard care in this patient group. Multicenter, multinational study increasing applicability of findings. Outcome assessors were blinded to treatment arm. Hematoma measurements were made with a standard protocol and central site adjudication. 12 hour NIHSS assessments were performed by health care professionals who were unaware of group assignments Limitations: Study funded, designed, and supervised by AstraZeneca Pharmaceuticals the maker of Andexanet alpha.  Although, this does not refute the findings of this study, it should make readers skeptical. Clinicians were not blinded to the treatment arm patients were randomized to. This may introduce bias particularly in terms of subsequent treatments (treatments outside of reversal are not detailed in the study). Primary endpoint is not patient centered. Convenience sample of patients which introduces bias. There are some baseline differences between groups and it’s hard to say how this may have influenced the results. Exclusion criteria are likely to be difficult for clinicians to assess real time leading to protocol violation (particularly items like planned surgery and recent thrombotic event). Dose adjustment for time from ingestion likely to lead to protocol violation as this info difficult to assess. Exclusion criteria: Removed the sickest patients. Discussion: The positive primary and secondary outcomes Both the primary (hematoma expansion) and secondary (anti-fac

Take Home Points: There are many causes of neutropenia, chemotherapy being by far the most dangerous. Febrile neutropenia is a condition conveying high mortality. Early administration of antibiotics is the only factor known to reduce this mortality. For a patient with neutropenic fever, remember that the body’s own flora is the greatest danger. Isolate, but do not wait to initiate treatment. Check old blood cultures and obtain new cultures prior to starting treatment. Identify low risk patients and send them home with PO antibiotics and close oncology follow-up in conjunction with your oncologist. REBEL Core Cast 122.0 – Neutropenic Fever Click here for Direct Download of the Podcast. Neutropenia and Neutropenic Fever Neutropenia: An absolute neutrophil count less than 500 cells/mm3 or less than 1000 cells/mm3 with a predicted decline to less than 500 cells/mm3 ANC = WBC x (neutrophil% + band%) Mild: 1000 – 1500 Mod: 500 – 1000 Severe: 100 – 500 Profound: <100 Background Neutrophils directly combat infection and are important to coordinating the body’s overall immune response. The loss of these cells leads to immunosuppression as well as decreased responsiveness of the immune system as a whole Patients with neutropenia will not only get very sick very quickly, but also will have blunted immune response and may not localize signs of infection well Fever or malaise may be their only presenting symptoms. Patients with hematologic malignancies are at highest risk for suffering profound and prolonged neutropenia. Particularly high risk are those undergoing induction chemotherapy or stem cell transplant. Allogeneic stem cell grafting is higher risk than autologous. Neutropenic Fever:  Fever (one reading of 38.3C or sustained 38.0C) + ANC < 500 cells/mm3 or expected to fall to < 500 cells/mm3 within the next 48 hours Common problem during chemotherapy: 10-50% of patients with solid malignancy and >80% of patients with hematologic malignancy will experience at least one episode of neutropenia (IDSA 2010, Klastersky 2004) Associated with high morality: ~90% without antibiotics (Perron 2014, Klastersky 2009) ~2-21% when treated with early antibiotics (Clarke 2011, Kruderer 2006) Higher mortality rates with co-morbidities and hematologic malignancies Time to antibiotic administration has been shown to directly impact mortality (Perron 2014, Rosa 2014, Marín 2015) Causes of neutropenia (Gibson 2014): Overconsumption Sepsis Autoimmune disease (SLE, rheumatoid arthritis, etc) Underproduction by bone marrow Malnutrition – alcoholism, anorexia, etc Myelodysplastic syndrome Post-viral: varicella, measles, rubella, influenza, hepatitis, Epstein-Barr virus, HIV Drug induced: clozapine, methimazole, sulfasalazine, bactrim, b-lactam antibiotics, NSAIDs, ticlopidine, cephalosporins, chemotherapy Chemotherapy: Includes many drugs and drug regimens, all with the goal of killing rapidly dividing cells. Of note, this particularly affects: Cancer cells – this is the reason chemotherapy works as treatment Neutrophils – with a life cycle of only 1-6 days, their numbers are impacted dramatically by chemotherapy Mucosa – destruction of dividing cells thins mucosal barriers, putting these patients at high risk for mucositis and bacterial invasion This creates a dangerous situation where the body’s barriers against bacterial invasion are broken down and, thus, the ability to combat infection is severely blunted. Antibiotics are effectively the only thing standing between these patients and overwhelming sepsis. Pathogens (Gudiol 2013): The pathogens responsible for neutropenic fever have changed over time. Initially, Gram (-) organisms translocated from the gut caused majority of cases of neutropenic fever This changed in the 1990s. Gram(+) infections became more common due to more fluoroquinolone prophylaxis against Gram (-) organisms and due to more prevalent use of indwelling catheters for outpatient treatment Over the past decade, there has been a resurgence of Gram (-) organisms due to increasing antibiotic resistance, particularly multidrug resistant E coli and klebsiella Given the increasing rates of antibiotic resistance, antibiotic stewardship is becoming increasingly important In the ED, we can contribute to antibiotic stewardship by checking old cultures and obtaining new ones prior to initiation of antibiotics ED Evaluation  and Management: Resuscitate if necessary Patients with neutropenic fever may rapidly progress to septic shock. Give appropriate fluids, vasopressors, and antibiotics. Antibiotics need to be given as quickly as possible if unstable Perform a complete review of systems and physical exam looking for signs of focal infection Basic Blood Work CBC, BMP, LFTs, bilirubin levels Blood cultures If indwelling catheter present: 1 set from each line of indwelling catheter + 1 peripheral set If no indwelling catheter pre

Background: The holy grail of outcomes in OHCA is survival with good neurologic outcome.  The only interventions proven to increase this outcome are high quality CPR and defibrillation in shockable rhythms.  Ventilation is also an important component of resuscitation in OHCA.  Excess minute ventilation can adversely affect hemodynamics due to increased intrathoracic pressure (i.e. decreased venous return). Additionally, low CO2 levels from hyperventilation can lead to cerebral vasoconstriction which could lead to worsened secondary brain injury.       Most organizations recommend adults to be ventilated with tidal volumes of 500 to 600mL/breath during ongoing CPR.  Large adult BVMs can have maximum tidal volumes of ≈1500mL and deliver about 750mL per one handed ventilation.  Simulation studies have shown that health care professionals often provide minute ventilation well above these recommended ranges.       One of the recommendations from many experts to mitigate the perceived risk of large adult BVMs is using smaller adult BVMs.  This change would result in decreasing the maximum volume from 1500 to 1000mL and an expected delivered tidal volume from 750 to 450mL/breath  (much more inline with recommended ranges). However, evidence that this approach makes is difference is lacking. REBEL Cast 126: Should We Not Be Recommending Small Adult BVMs in OHCA? Click here for Direct Download of the Podcast Paper: Snyder BD et al. Association of Small Adult Ventilation Bags with Return of Spontaneous Circulation in Out of Hospital Cardiac Arrest. Resuscitation 2023. PMID: 37805062 Clinical Question: Is large adult BVM or small adult BVM associated with more ROSC in adult patients treated with advanced airway placement for nontraumatic OHCA? What They Did: Retrospective, observational cohort analysis of prospectively obtained data from a single urban EMS system Evaluating adults treated with advanced airway placement for nontraumatic OHCA Jan 2015 to Dec 2021 Changed from large adult BVMs to small adult BVMs in summer of 2017 (3 month crossover period was allowed and excluded from analysis) Used a Mercury medical CPR-2 small ventilation bag Compared rates of ROSC, ventilation rate, and mean end tidal carbon dioxide (ETCO2) by minute before and after small adult BVM implementation Outcomes: Primary: ROSC at the end of EMS care (i.e. Arrival to ED or terminated efforts in the field) Secondary: Ventilation rate Mean end-tidal CO2 (ETCO2) during CPR Inclusion: Adult patients with nontraumatic OHCA Treated with an advanced airway (i.e. Endotracheal intubation or iGel) Exclusion: Age <18 years Received basic life support only Termination of resuscitation due to advanced directives ALS interventions prior to EMS arrival Insufficient capnography data Cricothyrotomy Advanced airway placed while patient had spontaneous circulation Airway was managed with BVM only Did not receive CPR while under EMS ALS care Results: 1994 Patients included in analysis 1331 (67%) treated with small adult BVM 663 (33%) treated with large adult BVM 21% had an initial shockable rhythm ROSC Small Adult BVM: 33% Large Adult BVM: 40% uOR 0.74; 95% CI 0.61 to 0.90; P = 0.003 After adjustment for age, sex, witnessed arrest, bystander CPR, and initial rhythm this finding remained statistically significant (aOR 0.74; 95% CI 0.61 to 0.91) Ventilation rates did not differ between cohorts (≈12BPM) ETCO2 Small Adult BVM: 36.9 +/- 19.2mmHg Large Adult BVM: 33.2 +/- 17.2mmHg P <0.01 Strengths: Written records are compared to cardiac monitor files and audio recordings to adjudicate differences before integrating information into the registry Intubations confirmed with ETCO2 Took into account the COVID-19 pandemic time period Also took into account the potential for trends over time by visualizing the incidence of ROSC by month over a seven year period and found no significant change in the slope before and after the implementation of the small adult BVM Limitations: Only included patients that were intubated with an endotracheal tube or iGel (these results may not apply in patients without these devices) There were some confounding baseline differences (explained more in discussion) Unclear what other interventions were performed in terms of ACLS medications or what the specific causes of the cardiac arrest were from This was a before and after study not allowing for a control group. Before and after studies can introduce numerous biases particularly if other pieces of care changed between the two time periods. (Can also go in the discussion) The actual tidal volume delivered was not measured in this trial and therefore the delivered minute ventilation is unknown As this is a retrospective study, we can only show association, BUT NOT causation of the size of the adult BVM affecting ROSC outcomes Discussion: There are some key BASELINE DIFFERENCES that could

Take Home Points Acute rhinosinusitis is a clinical diagnosis The vast majority of acute rhinosinusitis cases are viral in nature and do not require antibiotics Consider the use of antibiotics in select groups with severe disease or worsening symptoms after initial improvement. REBEL Core Cast 121.0 – Acute Sinusitis Click here for Direct Download of the Podcast. Definition: Acute rhinosinusitis (ARS) – Symptoms for less than four weeks Subacute rhinosinusitis – Symptoms for 4 to 12 weeks Chronic rhinosinusitis – Symptoms persisting greater than 12 weeks Recurrent acute rhinosinusitis – Four or more episodes of ARS per year, with interim symptom resolution Epidemiology: (Anon 2004) 20 million cases of sinusitis annually in the US, costing $3.5 billion/year Source of 1 in 5 antibiotic prescriptions for adults Presentation: Sinusitis is most commonly diagnosed by clinical symptoms Common symptoms Purulent nasal discharge Nasal congestion Facial pain or pressure, especially over a sinus or unilaterally Anosmia Hyposmia Fever Cough Fatigue Maxillary pain Ear pressure or fullness. Classification of Sinusitis: ●Acute viral rhinosinusitis (AVRS) ARS with viral etiology (i.e. rhinovirus, influenza, and parainfluenza) Most common form of ARS ●Uncomplicated acute bacterial rhinosinusitis (ABRS) ARS with a bacterial etiology without clinical evidence of extension outside the paranasal sinuses and nasal cavity Bacterial superinfection: 0.5-2% of all ARS ●Complicated acute bacterial rhinosinusitis ARS with bacterial etiology with clinical evidence of extension outside the paranasal sinuses and nasal cavity Sinusitis: Viral vs. Bacterial: Color change in sputum does not determine whether infection is viral or bacterial Viral infections Tend to begin resolution by 7-10 days Rarely have associated fevers If fever present, usually only in the first 48 hours. Guidelines for diagnosing ABRS are Presence of URI/cold symptoms that Don’t improve after 10 days Worsen after 5-7 days of improvement Severe symptoms including high fever, purulent discharge or facial pain for 3-4 days The Data Behind Antibiotic Use Clinically diagnosed acute sinusitis Multiple studies show the same cure rate at 7 days, but improved cure rate at 7-14 days for those who use antibiotics (Lemiengre 2012, Berg 1986, Gwaltney 1996) Overall Treatment Effect NNT = 18 Overall Harm NNH = 8 (mostly GI side effects) Radiographically-diagnosed acute sinusitis (Ahovuo-Saloranta 2008) Endpoint: clinical cure at 7-15 days NNT = 15 NNH = 8 IDSA Recommendations for Antibiotic Treatment (Chow 2012) Patients that should be treated Persistent symptoms w/o improvement (> 10 days) Severe symptoms (> 3-4 days) Worsening (“double-sickening”) (> 3-4 days) Antimicrobials 1st Line Amoxicillin 875 mg PO BID X 5-7 days Doxycycline 100 mg PO BID X 5-7 days 2nd Line Amoxicillin/Calvulanate 875/125 mg PO BID X 5-7 days Levofloxacin 500 mg PO Q24 X 5 days Bottom Line: Given the risk for adverse events associated with antibiotic use, the growing specter of resistance and the lack of significant differences in outcomes with antibiotic use, it is better to avoid antibiotics in most patients with ARS. Antibiotics should be considered in those with severe disease and in immunocompromised patients Take Home Points Acute rhinosinusitis is a clinical diagnosis The vast majority of acute rhinosinusitis cases are viral in nature and do not require antibiotics Consider the use of antibiotics in select groups with severe disease or worsening symptoms after initial improvement. References Anon JB et al. Antimicrobial treatment guidelines for acute bacterial rhinosinusitis. Otolaryngol Head Neck Surg 2004; 130(Suppl 1): 1-45. PMID: 14726904 Lemiengre MB et al. Antibiotics for Clinically Diagnosed Acute Rhinosinusitis in Adults. Cochrane Database Syst Rev 2012. PMID: 23076918 Berg O et al. Occurence of asymptomatic sinusitis in common cold and other acute ENT-infections. Rhinology 1986; 24(3): 223-5. PMID: 3775189 Gwaltney JM. Acute community-aquired sinusitis. Clin Infect Dis 1996; 23(6): 1209-23. PMID: 8953061 Ahovuo-Saloranta A et al. Antibiotics for acute maxillary sinusitis. Cochrane Database Syst Rev 2008. PMID: 18425861 Chow AW et al. IDSA Clinical practice guideline for acute bacterial rhino sinusitis in children and adults. Clin Infect Dis 2012; 54(8): e72-e112. PMID: 22438350 Read More The NNT.com: Antibiotics for Clinically Diagnosed Acute Sinusitis in Adults The NNT.com: Antibiotics for Radiologically-Diagnosed Acute Maxillary Sinusitis Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie) The post REBEL Core Cast 121.0 – Acute Sinusitis appeared first on REBEL EM - Emergency Medicine Blog.

Podcast Direct Download: Link Release Date: April 16th, 2024 Show Notes The Visible Voices Podcast Dr. Glaucomflecken: Power of Ultrasound with Emergency Medicine Dr. Resa Lewiss Adaira I Landry MD Resa E Lewiss MD is a Professor of Emergency Medicine at the University of Alabama at Birmingham. A TEDMED speaker and TimesUp Healthcare founder, she’s an internationally renowned point-of-care ultrasound educator and champion for diverse, equitable, and inclusive workplaces. She attended college at Brown, medical school at Penn, Emergency Medicine residency at Harvard, and fellowship at Mount Sinai St. Luke’s Roosevelt.  She led point-of-care ultrasound sections at St. Luke’s Roosevelt, the University of Colorado, and Thomas Jefferson. A physician healthcare design consultant for Perkins&Will, her design focus has been ultrasound hardware and workflows. She’s helped to redesign the built environment of a Harvard ICU and an infectious diseases unit in Malawi. As host and founder of the Visible Voices Podcast, she’s interviewed dozens of subject matter experts in healthcare, equity, and current trends. Her writings are published in the popular press and scientific journals, such as Harvard Business Review, Slate, Nature, and Fast Company. Her new book, MicroSkills : Small Actions, Big Impact is forthcoming from HarperCollins in 2024. Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie) The post REBEL EM Book Club – MicroSkills appeared first on REBEL EM - Emergency Medicine Blog.