
Emergency Medical Minute
Our near daily podcasts move quickly to reflect current events, are inspired by real patient care, and speak to the true nature of what it's like to work in the Emergency Room or Pre-Hospital Setting. Each medical minute...
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On the show
- Aaron Lessen, MD7 eps
- Travis Barlock, MD6 eps
- Alec Coston, MD1 ep
Also: Taylor Lynch MD, Taylor Lynch, MD, Meghan Hurley, MD, Dan Orbidan, Dr. Travis Barlock
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Based on 1 signal.
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By chart position
- 🇺🇸United States · MedicineHOME#9917K to 89K
- 🇲🇾MY · Medicine#171.4K to 7.2K
- 🇨🇦Canada · Medicine#761.2K to 6.6K
- 🇳🇿New Zealand · Medicine#30743 to 3.9K
- 🇸🇪Sweden · Medicine#48644 to 3.4K
- Per-Episode Audience
Est. listeners per new episode within ~30 days
23K to 124K🎙 ~2x weekly·1,000 episodes·Last published 2d ago - Monthly Reach
Unique listeners across all episodes (30 days)
47K to 248K🇺🇸72%🇲🇾6%🇨🇦5%+10 more - Active Followers
Loyal subscribers who consistently listen
26K to 136K
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* Data sourced directly from platform APIs and aggregated hourly across all major podcast directories.
| Date | Episode | Topics | Guests | Brands | Places | Keywords | Sponsor | Length | |
|---|---|---|---|---|---|---|---|---|---|
| 10/26/26 | Podcast 1028: POCUS Before Cath in Pediatric Patients | Contributor: Aaron Lessen, MD Educational Pearls: Febrile work-ups in the emergency department require obtaining a urine sample to assess for UTI. In non-toilet trained children, this often means using catheterization. Depending on the volume of urine in the bladder, there may not be enough present to get an adequate sample. Performing a bladder scan before catheterization may be helpful in determining if there is enough urine there in the first place to get a sample. A recent systematic review and meta-analysis of three randomized control trials found that performing a POCUS prior to catheterization in 337 children aged 36 months and younger led to higher success in obtaining a sample. The success of getting a sample on the first attempt increased from 72.5% to 89.7%. The rate of dry taps decreased from 23.9% to 3.6%. POCUS before catheterization is an easy tool providers can use to ensure an adequate first attempt and reduce unnecessary discomfort for the child. References: Vieira da Silva HF, Watanabe ET, Tavares MC, Ramos Bicalho AC, Ferraro LSD, Simões E Silva AC. Point-of-care ultrasound for pediatric urethral catheterization: a systematic review and meta-analysis of randomized controlled trials. Acad Emerg Med. 2026;33(6):e70342. doi:10.1111/acem.70342 Summarized by Ashley Lyons, OMS4 | Edited by Ashley Lyons & Ahmed Abdel-Hafiz, NREMT-P Donate: https://emergencymedicalminute.org/donate/ Join our mailing list: http://eepurl.com/c9ouHf | 1m 58s | ||||||
| 10/19/26 | Podcast 1027: Oculocardiac Reflex | Contributor: Taylor Lynch, MD Educational Pearls: What is the oculocardiac reflex? The oculocardiac reflex occurs when pressure or traction is put onto the globe of the eye or extraocular muscles that causes increased stimulus to the ophthalmic division of the trigeminal nerve (Cranial Nerve V). The trigeminal nerve then has a reflex arc with the vagus nerve (Cranial Nerve X) causing it to be stimulated and create downstream outward parasympathetic effects. The activated vagus nerve will cause an inhibitory signal to be sent to the heart, causing bradycardia. This bradycardia can also be present as certain arrhythmias like AV blocks. What are the patient presentations and treatment considerations for the oculocardiac reflex? In the emergency department or pre-hospital field it can present in patients with frank orbital trauma with otherwise unexplained bradycardia including: blow-out fractures, retrobulbar hematoma, foreign bodies in the eye, or be caused from eye-dressings placed too tightly. For treatment, the most important step is recognizing the condition and removing the offending agent that may be causing the reflex, and seeking to reduce pressure. It is also important to have the patient on cardiac monitoring. If that is not effective, atropine can be considered at 0.5mg repeat doses to improve the bradycardia, but ultimately trying to end the reflex arc is important. References Chua AW, Chua MJ, Leung H, Kam PC. Anaesthetic considerations for strabismus surgery in children and adults. Anaesth Intensive Care. 2020;48(4):277-288. doi:10.1177/0310057X20937710 Arnold RW. The Oculocardiac Reflex: A Review. Clin Ophthalmol. 2021;15:2693-2725. doi:10.2147/OPTH.S317447 Summarized by Dan Orbidan, OMS3 | Edited by Dan Orbidan & Ahmed Abdel-Hafiz, NREMT-P Donate: https://emergencymedicalminute.org/donate/ Join our mailing list: http://eepurl.com/c9ouHf Golf Fundraiser: https://www.zeffy.com/en-US/ticketing/emergency-medical-minute-charity-golf--2026 | 2m 53s | ||||||
| 10/17/26 | Podcast 1026: Esophageal Balloon Tamponade Devices | Contributor: Jeffrey Olson, MD Educational Pearls: What are they? A flexible balloon and suction tube that we insert into the esophagus and into the stomach to stop bleeding. When to use? Typically used for variceal bleeding. Use whenever the patient is too unstable to be transferred to more definitive therapy. What are the different types? Linton - Nachlas Tube Single gastric balloon with a suction port for the stomach and sometimes a suction port for the esophagus. Sengstaken - Blakemore Tube Gastric balloon and esophageal balloon with only a gastric suction port Minnesota Tube Both gastric and esophageal balloon and both gastric and esophageal suction ports How do you place one? Before placement Secure the airway first in a patient with massive ongoing hematemesis Insertion Fully lubricate the tube. Remove the white caps from the gastric and esophageal inflation ports. Test your balloons by placing them in the water and inflating them using your syringe. Place your three-way stopcocks on your esophageal and gastric inflation ports. Insert the tube similar to an OG tube until you have reached the 50 cm mark for the gastric balloon Use a slip syringe at the gastric aspiration site and auscultate to confirm that you are in the stomach. Then fill the gastric balloon with 50 cc of air. Verify the placement of the gastric balloon with a chest x-ray. (You can also pre-check with ultrasound) Fully inflate the gastric balloon Blakemore: 250ccs Minnesota: 450-500ccs Apply traction to the tube by tying a roller bandage to the end of it and then the other end to a 1L bag of IV fluids. Then hang the roller bandage over an IV pole. Place the nasogastric tube down to the pre-measured level above the gastric balloon and suction the esophageal space. If there is continued bleeding coming from the nasogastric tube then you will need to inflate the esophageal balloon. Note that Minnesota tubes already have their own esophageal suction port and will NOT need this NG tube placement to suction the esophagus. Use a "manometer" to inflate the esophageal balloon to 30mmHg. If bleeding persists, you can go to a maximum of 45mmHg What are some tricks? Using silk ties to add an accessory NG tube to add an extra suction port to a Blakemore tube Using a bougie to help advance Put the tube on ice to increase stiffness and make it easier to pass Use Macgills to help advance Use a laryngoscope Use endoscopic biopsy forceps threaded down the gastric port What does the data say? "The overall success rate of initial hemostasis with [Blakemore] tube was 75.8. Rebleeding rate after successful initial hemostasis with [Blakemore] tube was 22.0%, and esophageal rupture occurred in 6.1%. Mortality within 30 days was 42.4%" (Choi, 2017) References Choi JY, Jo YW, Lee SS, Kim WS, Oh HW, Kim CY, Yun EY, Kim JJ, Lee JM, Kim HJ, Kim HJ, Kim TH, Jung WT, Lee OJ, Kim RB. Outcomes of patients treated with Sengstaken-Blakemore tube for uncontrolled variceal hemorrhage. Korean J Intern Med. 2018 Jul;33(4):696-704. doi: 10.3904/kjim.2016.339. Epub 2017 Nov 10. PMID: 29117668; PMCID: PMC6030415. https://www.aliem.com/trick-inflating-esophageal-balloon-blakemore-minnesota-tube-without-manometer/ https://www.tamingthesru.com/blog/air-care-series/balloon-tamponade-of-variceal-hemorrhage https://radiopaedia.org/articles/esophageal-balloon-tamponade-device https://simkit.co/blakemore-minnesota-and-linton-tube-tips-and-tricks/ https://www.bjaed.org/article/S2058-5349%2817%2930055-0/fulltext Summarized by Jeffrey Olson MD | Edited by Jeffrey Olson MD Special thanks to Dr. Travis Barlock, Dr. Evan Fisch, and the Corewell Health East - William Beaumont Emergency Medicine Residency Program for their contributions in researching for this episode. Donate: https://emergencymedicalminute.org/donate/ Join our mailing list: http://eepurl.com/c9ouHf Golf Fundraiser: https://www.zeffy.com/en-US/ticketing/emergency-medical-minute-charity-golf--2026 | 7m 59s | ||||||
| 10/12/26 | Podcast 1025: Post intubation Sedation | Podcast 1025: Post intubation Sedation Contributor: Aaron Lessen, MD Educational Pearls: Experts suggest that anyone who is put on a ventilation should be given sedation. When acquiring Rapid Sequence Intubation (RSI) medications and kits, one should also plan their sedation strategy and always consider the patient becoming unstable hypotensive after their intubation. References Needleman R, Dyer S, Martinez KA, Routsolias JC. Optimizing administration and timing of post intubation analgesia and sedation in the Emergency Department. Journal of Emergency Nursing. 2025;51(2):215-219. doi:10.1016/j.jen.2024.10.011 Baumgartner K, Fuller BM. Post-intubation sedation and analgesia in the emergency department: The basics and beyond. Emergency Medicine Clinics of North America. 2026;44(4):583-596. doi:10.1016/j.emc.2026.02.004 Rosenberg H, Hendin A, Rosenberg E. Just the Facts: Postintubation sedation in the emergency department. CJEM. 2020;22(6):764-767. doi:10.1017/cem.2020.437 Romagnoli, S., Matta, B., Driver, B.E. et al. A plea for enhanced monitoring of depth of sedation in patients who are intubated and ventilated. Crit Care 28, 342 (2024). https://doi.org/10.1186/s13054-024-05105-9 Summarized by Aaryn David | Edited by Aaryn David & Ahmed Abdel-Hafiz, NREMT-P Donate: https://emergencymedicalminute.org/donate/ Join our mailing list: http://eepurl.com/c9ouHf Golf Fundraiser: https://www.zeffy.com/en-US/ticketing/emergency-medical-minute-charity-golf--2026 | 2m 44s | ||||||
| 10/5/26 | Podcast 1024: Caffeine Toxicity | Contributor: Taylor Lynch, MD Educational Pearls: Excessive caffeine intake can be dangerous. For normal adults, the toxicity level starts at 1000mg, which is equivalent to about 10 cups of coffee or 5 celsius drinks. For normal adults, lethal levels are about 5-10 grams, which is equivalent to about 50-100 cups of coffee. Most of these outcomes are not from drinking caffeine, but instead concentrated caffeine pills. For children, toxic levels are 15mg per kg of the child. Within the last 10 years 20-40 deaths due to caffeine intake have been reported. This may be lower than the actual number due to cardiac arrests that potentially could have been caused from caffeine intake. Clinical presentation of caffeine toxicity can present in many ways. Most common symptoms include agitation and jitteriness The far end of the spectrum includes seizures, tachydysrhythmias, and eventually cardiovascular collapse. Caffeine is a part of the methylxanthine class. Caffeine is a phosphodiesterase inhibitor, which causes the release of calcetamines that act on your beta-2 receptors. This activates the sodium potassium ATPase and causes potassium to shift intracellular. The clinical presentation of this mechanism is a patient with low potassium and agitation. Treatments for toxic caffeine levels include: Replacing potassium, but slowly since the total potassium levels in the body are normal and will eventually return to normal once the caffeine wears off. Benzodiazepines Activated charcoal Dialysis, since caffeine is dialyzable References National Center for Biotechnology Information. "PubChem Compound Summary for CID 2519, Caffeine" PubChem, https://pubchem.ncbi.nlm.nih.gov/compound/Caffeine. Accessed 9 July, 2026. Murray A, Traylor J. Caffeine Toxicity. [Updated 2025 Feb 6]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2026 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK532910/ Cyril Willson, The clinical toxicology of caffeine: A review and case study, Toxicology Reports, Volume 5, 2018, Pages 1140-1152, ISSN 2214-7500, https://doi.org/10.1016/j.toxrep.2018.11.002. Summarized by Aaryn David | Edited by Aaryn David & Ahmed Abdel-Hafiz, NREMT-P Donate: https://emergencymedicalminute.org/donate/ Join our mailing list: http://eepurl.com/c9ouHf Golf Fundraiser: https://www.zeffy.com/en-US/ticketing/emergency-medical-minute-charity-golf--2026 | 3m 12s | ||||||
| 9/28/26 | Podcast 1023: Torsades de pointes | Contributor: Aaron Lessen, MD Educational Pearls: Case review of a patient with recurrent episodes of syncope and shortness of breath, during which she is found to have intermittent runs of polymorphic ventricular tachycardia Torsades de pointes is polymorphic ventricular tachycardia occurring in the setting of a prolonged QT/QTc Risk of torsades increases substantially when QTc exceeds 500ms Causes: Common reversible causes include QT-prolonging medications, hypokalemia, hypomagnesemia, hypocalcemia, bradycardia, and structural heart disease Congenital causes of a prolonged QT interval are primarily inherited genetic mutations affecting cardiac myocyte ion channels leading to delayed ventricular repolarization Treatment: Stop any QT-prolonging medications and correct electrolytes IV magnesium to suppress recurrent torsades Increasing the heart rate with isoproterenol or temporary pacing can prevent the pauses that trigger recurrent episodes If the rhythm degenerates into ventricular fibrillation → defibrillate References Wigginton JG, Agarwal S, Bartos JA, Coute RA, Drennan IR, Haamid A, Kudenchuk PJ, Link MS, Panchal AR, Pelter MM, Del Rios M, Rodriguez AJ, Perman SM, Sanko S, Kotini-Shah P, Kurz MC. Part 9: Adult Advanced Life Support: 2025 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2025 Oct 21;152(16_suppl_2):S538-S577. doi: 10.1161/CIR.0000000000001376. Epub 2025 Oct 22. PMID: 41122884. Summarized by Meg Joyce, MS3 | Edited by Meg Joyce & Ahmed Abdel-Hafiz, NREMT-P Donate: https://emergencymedicalminute.org/donate/ Golf Fundraiser: https://www.zeffy.com/en-US/ticketing/emergency-medical-minute-charity-golf--2026 | 5m 36s | ||||||
| 9/21/26 | Podcast 1022: Emergent Dialysis | Contributor: Taylor Lynch, MD Educational Pearls: When a patient who missed dialysis presents to the emergency department, our clinical concern is who needs to be admitted to the hospital for emergent dialysis and who can wait for their next regularly scheduled session. Dialysis sessions typically occur on Monday, Wednesday, and Friday, or Tuesday, Thursday, and Saturday. Acronym for indications for emergent dialysis: AEIOU Acidosis Patients may have an underlying cause for acidosis such as sepsis or DKA. Treat the underlying cause, but if the acidosis is unable to be corrected, the patient needs dialysis. Electrolytes Most commonly elevated is potassium. In general, dialysis patients tend to have higher potassium levels, so don't just treat the number. Look for potassium greater than 6.5 or if EKG changes are present. Ingestion Intoxication with substances such as Lithium, Ethylene Glycol, Methanol, Salicylates. Overload Patients may present with evidence of fluid overload such as new oxygen requirement or pulmonary edema. If they are making urine, treat with diuretics, but if unresponsive to medical therapy, they will require dialysis. Uremia Build-up of nitrogenous waste products in the blood, which is indicated by an elevated BUN. Patients may develop complications such as altered mentation or pericardial effusions and subsequent cardiac tamponade. Keep in mind creatinine itself is not an indication for emergent dialysis. Serves as a surrogate marker of kidney function. Can be high or low depending on muscle mass or kidney filtration, and the patient may or may not need dialysis. References: Jentzer JC, Bihorac A, Brusca SB, et al. Contemporary Management of Severe Acute Kidney Injury and Refractory Cardiorenal Syndrome: JACC Council Perspectives. J Am Coll Cardiol. 2020;76(9):1084-1101. doi:10.1016/j.jacc.2020.06.070 Summarized by Ashley Lyons, OMS4 | Edited by Ashley Lyons & Ahmed Abdel-Hafiz, NREMT-P Donate: https://emergencymedicalminute.org/donate/ Join our mailing list: http://eepurl.com/c9ouHf | 4m 15s | ||||||
| 9/14/26 | Podcast 1021: Pulmonary Edema From Naloxone Administration | Contributor: Travis Barlock, MD Educational Pearls: What is pulmonary edema? Pulmonary edema is the accumulation of fluid initially in the interstitium of the lungs, that when severe enough can also accumulate in the alveolar air sacs. It develops when the rate of fluid filtration through the pulmonary vasculature out-paces the lymphatics ability to drain the fluid. There are 2 theories for what causes pulmonary edema in the setting of naloxone administration: catecholamine surge vs negative pressure/barotrauma Catecholamine Surge : Naloxone administration precipitates an acute opioid withdrawal in which epinephrine and norepinephrine surge causing marked vasoconstriction on both the heart and the lungs Negative Pressure/Barotrauma: This mechanism is not directly naloxone related but may be confounded by opioid effects. High dose synthetic opioids can induce sustained laryngospasm that is not mu-opioid mediated (thus not easily reversed by naloxone). With rapid awakening, respiratory muscles induce a negative pressure in the thoracic cavity against a closed glottis. This results in an alveolar barotrauma and a transudative pulmonary edema. What is the treatment for pulmonary edema secondary to opioid overdose reversal? Positive pressure ventilation is the mainstay treatment (CPAP/BiPAP) with oxygen supplementation. Importantly, diuretics are not recommended. The patient is not fluid overloaded like in the case of other pulmonary edemas, and diuresing the patient can worsen kidney injury which is already at an increased risk in opioid overdoses (rhabdomyolysis in particular). References: Saari TI, Strang J, Dale O. Clinical Pharmacokinetics and Pharmacodynamics of Naloxone. Clin Pharmacokinet. 2024;63(4):397-422. doi:10.1007/s40262-024-01355-6 DailyMed - NALOXONE HYDROCHLORIDE injection, solution. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=201fdedf-1736-4e52-9d7d-de14292547fd Boyer EW. Management of Opioid Analgesic Overdose. New England Journal of Medicine. 2012;367(2):146-155. doi:10.1056/NEJMra1202561 Dezfulian C, Orkin AM, Maron BA, et al. Opioid-Associated Out-of-Hospital Cardiac Arrest: Distinctive Clinical Features and Implications for Health Care and Public Responses: A Scientific Statement From the American Heart Association. Circulation. 2021;143(16):e836-e870. doi:10.1161/CIR.0000000000000958 Kienbaum P, Thurauf N, Michel M, Scherbaum N, Gastpar M, Peters J. Profound Increase in Epinephrine Concentration in Plasma and Cardiovascular Stimulation after [micro sign]-Opioid Receptor Blockade in Opioid-addicted Patients during Barbiturate-induced Anesthesia for Acute Detoxification Anesthesiology. 1998;88(5):1154-1161. doi:10.1097/00000542-199805000-00004 Summarized by Dan Orbidan, OMS3 | Edited by Dan Orbidan & Ahmed Abdel-Hafiz, NREMT-P Donate: https://emergencymedicalminute.org/donate/ Join our mailing list: http://eepurl.com/c9ouHf | 4m 24s | ||||||
| 9/7/26 | Podcast 1020: Benign Paroxysmal Positional Vertigo (BPPV) | Contributor: Alec Coston, MD Educational Pearls: Benign Paroxysmal Positional Vertigo (BPPV) Common inner ear condition that can cause dizziness Diagnosis of BPPV can help to avoid admissions and extra imaging Three categories: positional, horizontal, and anterior Positional is the most common Dizziness is not a positive indicator, a torsional nystagmus must be induced Dix's hallpike maneuver is done to diagnose and an epley maneuver is then used for treatment Horizontal Usually determined to be the case if the vertigo seems positional and the dix hallpike does not work. A supine roll test would then be done to help diagnose. Instead of a rotational nystagmus, a unilateral horizontal nystagmus is expected. The two patterns are termed geotropic and apogeotropic. Geotropic means the fast phase beats toward the ground, and is treated by a barbeque roll maneuver. Apogeotropic means the fast phase beats toward the ceiling, and is treated by Gufoni maneuver. Anterior is more rare Most cases require neuro consults Determined by attempting to induce a down-beating nystagmus, which is a higher risk nystagmus. Treatment is tilting their head back up in a similar way Inducing the nystagmus is not sided and is more central References You, P., Instrum, R. and Parnes, L. (2019), Benign paroxysmal positional vertigo. Laryngoscope Investigative Otolaryngology, 4: 116-123. https://doi.org/10.1002/lio2.230 Ling X, Zhao D-H, Shen B, Si L-H, Li K-Z, Hong Y, Li Z-Y and Yang X (2020) Clinical Characteristics of Patients With Benign Paroxysmal Positional Vertigo Diagnosed Based on the Diagnostic Criteria of the Bárány Society. Front. Neurol. 11:602. doi: 10.3389/fneur.2020.00602 Rah YC. Advances in Benign Paroxysmal Positional Vertigo: Updated Insights on Diagnostic Pitfalls and Management. J Audiol Otol. 2026 Jan;30(1):1-12. doi: 10.7874/jao.2025.00717. Summarized by Aaryn David | Edited by Aaryn David & Ahmed Abdel-Hafiz, NREMT-P Donate: https://emergencymedicalminute.org/donate/ Join our mailing list: http://eepurl.com/c9ouHf | 6m 31s | ||||||
| 8/31/26 | Podcast 1019: Trauma Blunt Cardiovascular Injuries (BCVI) | Contributor: Aaron Lessen, MD Educational Pearls: Blunt cerebrovascular injury (BCVI) BCVI is a traumatic injury to the carotid or vertebral arteries Patients may initially have no neurologic symptoms In some cases, a thrombus can form at the site of the injury and later cause ischemic stroke, sometimes hours after the original trauma CT angiography (CTA) of the neck is a useful screening tool for BCVI HIstorically, CTA was reserved for patients with high-risk mechanisms or neurologic symptoms CTA screening has expanded as understanding of BCVIs and their prevention progresses The Denver criteria were developed to identify patients with increased risk for BCVI High-risk findings include cervical spine injuries and severe facial or skull-base fractures Screening practices still vary between trauma centers, though expansion of proactive CTA is an increasingly common practice References Kim DY, et al. Evaluation and management of blunt cerebrovascular injury: A practice management guideline from the Eastern Association for the Surgery of Trauma. J Trauma Acute Care Surg. 2020. Biffl WL, et al. Screening for and treatment of blunt cerebrovascular injuries: Western Trauma Association critical decisions algorithm. J Trauma. 2009. Brommeland T, et al. Best practice guidelines for blunt cerebrovascular injury. Scand J Trauma Resusc Emerg Med. 2018. Harper PR, et al. Routine CTA screening identifies blunt cerebrovascular injuries missed by clinical risk factors. Trauma Surg Acute Care Open. 2022. Summarized by Sam Pahl | Edited by Sam Pahl & Ahmed Abdel-Hafiz, NREMT-P Donate: https://emergencymedicalminute.org/donate/ Join our mailing list: http://eepurl.com/c9ouHf | 3m 47s | ||||||
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| 8/24/26 | Podcast 1018: Occult Ventricular Fibrillation on Echocardiography | Contributor: Aaron Lessen, MD Educational Pearls: Big question in cardiac arrest: is the rhythm shockable? Shockable: ventricular fibrillation (VF) and pulseless ventricular tachycardia Non-shockable: asystole and pulseless electrical activity (PEA) Rhythm classification is typically based on ECG, but echocardiography can directly visualize myocardial fibrillation Occult VF: a rhythm that appears non-shockable on ECG but demonstrates VF on echocardiography A 2025 multicenter prospective study looked at 811 patients with out-of-hospital cardiac arrest 5.3% had occult VF detected by echocardiography Of the patients with occult VF: 81.4% had PEA on ECG 18.6% had asystole on ECG Patients with occult VF were less likely to receive defibrillation because their ECG suggested a nonshockable rhythm Clinical takeaway: echocardiography during cardiac arrest may reveal a potentially shockable rhythm hiding behind an apparently nonshockable ECG This identifies a subset of cardiac arrest patients who would otherwise be managed as PEA or asystole based on ECG References Gaspari R, Adhikari S, Gleeson T, Kapoor M, Lindsay R, Noble V, Nomura JT, Weekes A, Theodoro D. Occult Ventricular Fibrillation Visualized by Echocardiogram During Cardiac Arrest: A Retrospective Observational Study From the Real-Time Evaluation and Assessment for Sonography-Outcomes Network (REASON). J Am Coll Emerg Physicians Open. 2025 Jan 13;6(1):100028. doi: 10.1016/j.acepjo.2024.100028. PMID: 40012664; PMCID: PMC11853361. Summarized by Meg Joyce, MS3 | Edited by Meg Joyce & Ahmed Abdel-Hafiz, NREMT-P Donate: https://emergencymedicalminute.org/donate/ | 2m 20s | ||||||
| 8/17/26 | Podcast 1017: CPR Hand Placement | Contributor: Taylor Lynch, MD Educational Pearls: CPR is an important life-saving measure designed for anyone to perform. Chest compressions works by two mechanisms: Cardiac pump: Direct squeezing of the heart Thoracic pump: Increasing intrathoracic pressure, causing increased blood flow Proper hand placement per current AHA guidelines: Hands are placed in the center of the chest, on the lower half of the sternum A recent study challenged this approach, using TEE during chest compressions to visualize the cardiac structures being compressed. They found that when hands were placed ~1cm to the left of the sternum, this compressed the left ventricular outflow tract, potentially restricting forward blood flow. Hand placement ~4cm to the left of the sternum resulted in more effective compression of the left ventricle. While this is not yet reflected in AHA guidelines, the study presents an interesting finding that may influence how CPR is performed in the future. Key takeaway: Always prioritize administering high quality compressions. References: American Heart Association. 2025 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2025;152(23_suppl_1). doi:10.1161/CIR.0000000000001378. Chu S, Cheng C, Chang C, et al. Transesophageal echocardiography during CPR in patients with out-of-hospital cardiac arrest: the EXECT-CPR randomized clinical trial. JAMA Intern Med. 2026;186(5):557-566. doi:10.1001/jamainternmed.2026.0102. Summarized by Ashley Lyons, OMS4 | Edited by Ashley Lyons & Ahmed Abdel-Hafiz, NREMT-P Donate: https://emergencymedicalminute.org/donate/ Join our mailing list: http://eepurl.com/c9ouHf | 2m 51s | ||||||
| 8/10/26 | Podcast 1016: Hypokalemia | Contributor: Meghan Hurley, MD Educational Pearls: What is hypokalemia? Hypokalemia is when the measured blood level of potassium falls below 3.5 mEq/L (normal 3.5 - 5.2 mEq/L). Can generally be considered in mild (3.0 - 3.5 mEq/L); moderate (2.5 - 2.9 mEq/L); and severe ( Should be noted that blood levels of potassium can be low while total body potassium is normal due to intracellular shift by certain agents like β-2 agonists (e.g. Albuterol) or insulin. There is no appreciable loss of insulin despite hypokalemia being present in labs. What are the most common causes of hypokalemia? Medications are a predominant cause; mainly loop and thiazide diuretics. Gastrointestinal losses such as prolonged emesis or diarrhea (can occur in the setting of chronic illness and treatment such as chemotherapy patients with emesis). Other renal losses (e.g. hyperaldosteronism and renal tubular acidosis). A fun-fact renal loss: A compound found in some licorice (Glycyrrhizic acid) can inhibit 11-ß-hydroxysteroid dehydrogenase enzyme type 2 and cause mineralocorticoid excess. See a 2023 case study in references for Lethal Arrhythmia Induced by Licorice. What is a less common cause of hypokalemia? Hypokalemic Periodic Paralysis (HypoPP) is a genetic autosomal dominant channelopathy where patients leak potassium at rest causing a flaccid paralysis of muscle. Typically impacting legs more than arms, and proximal muscles more than distal muscles. Can be triggered carbohydrate rich meals, rest after exercise, febrile illness, and fasting. Male predominance, typically in early adulthood. Treatment is avoidance of triggers and supplementation with conservative oral potassium to avoid overcorrection during attacks. What are some symptoms and findings associated with hypokalemia? Patients may present with generalized weakness and fatigue. Highly crucial to monitor for EKG changes in the setting of hypokalemia. May notice flattening of T wave with the development of a U wave at certain potassium levels. The lower the potassium levels, the more likely a TU fusion can be seen. Prolongs QT interval which puts patients at risk for lethal arrhythmias. What are treatment considerations for hypokalemia? At milder levels of hypokalemia that are asymptomatic and a reversible cause is identified, oral repletion via potassium tablets should be considered. Patients may be a candidate to complete their course of treatment in the Emergency Room. At higher symptomatic levels with distinct EKG changes, more aggressive repletion (including IV Potassium) should be considered. Patients may be candidates for admission. Always monitor and replace magnesium levels as well, as they tend to follow potassium levels as well. Consider intracellular shifts as a source of hypokalemia to avoid risk of overcorrection into hyperkalemia. Hypokalemia can cause deadly heart rhythms such as ventricular fibrillation and ventricular tachycardia including Torsades Des Pointes that will be refractory to defibrillation. Treatment considerations at this point include: Consideration of esmolol Double Sequential Defibrillation Extracorporeal Membrane Oxygenation (ECMO). Key takeaways? Hypokalemia is most often associated with medication side effects or total volume loss from emesis or diarrhea. Depending on the degree of hypokalemia, different treatment considerations must be made. Monitor patient EKG closely for changes that can progress to lethal arrhythmias. References: Yannopoulos D, Bartos J, Raveendran G, et al. Advanced reperfusion strategies for patients with out-of-hospital cardiac arrest and refractory ventricular fibrillation (ARREST): a phase 2, single centre, open-label, randomised controlled trial. Lancet. 2020;396(10265):1807-1816. doi:10.1016/S0140-6736(20)32338-2 Cheskes S, Verbeek PR, Drennan IR, et al. Defibrillation Strategies for Refractory Ventricular Fibrillation. New England Journal of Medicine. 2022;387(21):1947-1956. doi:10.1056/NEJMoa2207304 Oswald S, Ravioli S, Schwarz C, Lindner G. Hypokalaemia in the emergency department: aetiology, diagnosis, and management. Swiss Medical Weekly. 2026;156(4):4767-4767. doi:10.57187/4767 Gao Z, Xing H, Zhang J, Chen S, Gao Z. Hypokalemic periodic paralysis: novel perspectives from genetic mutations to clinical management. Gene. 2026;999:150172. doi:10.1016/j.gene.2026.150172 Han EJ, Park JS. Lethal Arrhythmia Induced by Licorice. J Korean Med Sci. 2023;38(12):e107. doi:10.3346/jkms.2023.38.e107 Lee YH, Lee KJ, Min YH, et al. Refractory ventricular fibrillation treated with esmolol. Resuscitation. 2016;107:150-155. doi:10.1016/j.resuscitation.2016.07.243 Summarized by Dan Orbidan, OMS3 | Edited by Dan Orbidan & Ahmed Abdel-Hafiz, NREMT-P Donate: https://emergencymedicalminute.org/donate/ Join our mailing list: http://eepurl.com/c9ouHf | 6m 17s | ||||||
| 8/3/26 | Podcast 1015: Calcium in Hyperkalemia | Contributor: Meghan Hurley, MD Educational Pearls: What is hyperkalemia? Hyperkalemia is when the measured blood level of potassium reaches above 5.2 - 5.5 mEq/L (normal 3.5 - 5.2 mEq/L). What are common causes of hyperkalemia? Chronic or acute kidney disease. Medications that impact the Renin-Angiotensin-Aldosterone-System (RAAS). Hypoaldosteronism and primary adrenal insufficiency (Addison's Disease). What are concerns of hyperkalemia? The biggest concern with hyperkalemia is the impact on the cardiac conduction system. At differing levels of hyperkalemia, the patient may initially have peaked T waves, that then progress into a widening of the QRS complex which may eventually lead to a sine wave pattern. This increases risk for cardiac arrest with ventricular fibrillation, PEA, and asystole. What is the treatment algorithm for hyperkalemia? Works through a three-tier approach. First tier treatment is with a calcium agent (calcium gluconate or chloride). Thought for the longest time to "stabilize the cardiac membrane/action potential". Recent research shows the true mechanism of action is likely through acting on calcium dependent channels. Does not fix underlying hyperkalemia, but buys time for the heart. Second tier treatment is inducing intracellular potassium shift. Can be achieved through agents such as insulin (which may need to be bolused with glucose to prevent hypoglycemia), albuterol, or sodium bicarbonate. Third tier is potassium elimination If the patient is producing urine, loop or thiazide diuretics can be considered. Hemodialysis may also be considered based on patient condition. Long term (and slowest method of elimination) through fecal excretion. Unlikely to see benefits in emergency management. Key Takeaways? Hyperkalemia is a condition that can be brought on by primarily renal conditions and medication side effects. Careful attention must be paid to the patient's cardiac status, and urgent cardiac stabilization (though now we may know that calcium doesn't truly "stabilize" the cardiac membrane) must be performed to prevent deadly arrhythmias. Definitive management involves addressing the offending agent, offloading potassium, and stabilizing the patient long term. References: Geldermann N, Dzimiera J, Fischer H, Christ M. Acute hyperkalaemia in emergency care: evidence-based approaches. Emerg Med J. 2026;43(5):305-311. doi:10.1136/emermed-2025-215469 Piktel JS, Wan X, Kouk S, Laurita KR, Wilson LD. Beneficial Effect of Calcium Treatment for Hyperkalemia is Not Due to "Membrane Stabilization." Crit Care Med. 2024;52(10):1499-1508. doi:10.1097/CCM.0000000000006376 Hunter RW, Bailey MA. Hyperkalemia: pathophysiology, risk factors and consequences. Nephrol Dial Transplant. 2019;34(Suppl 3):iii2-iii11. doi:10.1093/ndt/gfz206 Summarized by Dan Orbidan, OMS3 | Edited by Dan Orbidan & Ahmed Abdel-Hafiz, NREMT-P Donate: https://emergencymedicalminute.org/donate/ Join our mailing list: http://eepurl.com/c9ouHf | 7m 04s | ||||||
| 7/27/26 | Podcast 1014: Eating and Drinking on Shift | Contributor; Aaron Lessen, MD Educational Pearls: A 2026 survey asked Canadian emergency medicine (EM) physicians about their eating and drinking habits while on shift. Among 527 respondents, 35% reported that they never or hardly ever ate during shifts, and 37% said the same about drinking water. Lack of time was the most commonly cited barrier, reported by 91% of respondents. Lack of available food, personal health goals, perceived mental clarity, and emergency department culture were also commonly identified factors. Physicians who did not eat or drink on shift often reported that this negatively affected their work. Years in practice were associated with eating more often while on shift, suggesting that newer physicians may be less likely to eat during shifts. A 2023 study by Kontrick et al. found that 89% of US-based EM residency programs did not have a dedicated meal break, which may help explain why early-career physicians are less accustomed to eating during clinical shifts. Studies outside of emergency medicine have also suggested that inadequate food and fluid intake can affect fatigue, mood, attention, and cognitive performance, though direct evidence in emergency department physicians and patient care remains limited. Future studies could examine whether physician eating and drinking habits during shifts are associated with patient outcomes and broaden the scope of this study to other emergency department providers, nurses, and technicians. References: Farquhar, Madeleine et al. "A lot on their plates? Examining the on-shift eating and drinking habits of Canadian emergency medicine physicians." CJEM vol. 28,1 (2026): 64-73. doi:10.1007/s43678-025-01044-8 Kontrick, Amy V et al. "Do emergency medicine residents have access to healthy food options during work hours?." AEM education and training vol. 7,4 e10890. 17 Jul. 2023, doi:10.1002/aet2.10890 Lemaire, Jane B et al. "Physician nutrition and cognition during work hours: effect of a nutrition based intervention." BMC health services research vol. 10 241. 17 Aug. 2010, doi:10.1186/1472-6963-10-241 Wittbrodt, Matthew T, and Melinda Millard-Stafford. "Dehydration Impairs Cognitive Performance: A Meta-analysis." Medicine and science in sports and exercise vol. 50,11 (2018): 2360-2368. doi:10.1249/MSS.0000000000001682 Summarized by Sam Pahl | Edited by Sam Pahl & Ahmed Abdel-Hafiz, NREMT-P Donate: https://emergencymedicalminute.org/donate/ Join our mailing list: http://eepurl.com/c9ouHf | 2m 10s | ||||||
| 7/20/26 | thoracotomytrauma+3 | Taylor Lynch, MD | — | — | thoracotomycardiac arrest+3 | — | 3m 57s | ||
| 7/13/26 | methamphetaminesedation+3 | Aaron Lessen, MD | Emergency Medical MinuteAm J Emerg Med | — | meth sedationemergency department+6 | — | 1m 58s | ||
| 7/6/26 | lethal animalsanaphylaxis+3 | Meghan Hurley, MD | HymenopteraWest Nile Virus | — | lethal animalsmosquitos+3 | — | 7m 19s | ||
| 6/29/26 | intubationemergency medicine+3 | Travis Barlock, MD | BEAM studyAcad Emerg Med+2 | — | first-pass successintubation+3 | — | 3m 39s | ||
| 6/22/26 | out of hospital callpatient management+3 | Dan OrbidanDr. Travis Barlock | Emergency Medical Minute | — | emergency medicinepatient care+3 | — | 35m 55s | ||
| 6/15/26 | medical discussionsneurology+3 | — | CarepointCarepoint's Emergency Physicians+1 | Neurology | Carepointneurology+3 | — | 36m 25s | ||
| 6/8/26 | UTI preventionvaginal estrogen+3 | Aaron Lessen, MD | Journal of UrologyAUA/CUA/SUFU+1 | — | UTIvaginal estrogen+5 | — | 1m 45s | ||
| 6/1/26 | acupuncturelow back pain+3 | Aaron Lessen, MD | — | — | acupuncturelow back pain+7 | — | 2m 02s | ||
| 5/25/26 | caffeine pharmacologyadenosine receptors+3 | Travis Barlock, MD | caffeinecoffee+5 | America | caffeineadenosine+5 | — | 4m 33s | ||
| 5/18/26 | cannabinoid pharmacologyendocannabinoid system+5 | Travis Barlock, MD | Δ9-Tetrahydrocannabinol (THC)2-arachidonoylglycerol (2-AG)+8 | — | cannabinoidsTHC+7 | — | 5m 02s | ||
| 4/27/26 | nasal intubationairway management+3 | Alec Coston, MD | — | — | nasal intubationoral intubation+6 | — | 9m 01s | ||
| 4/20/26 | elder agitationdementia+4 | Aaron Lessen, MD | — | — | elderly agitationdementia+5 | — | 3m 35s | ||
| 4/13/26 | pulmonary embolismrisk assessment+4 | Aaron Lessen, MD | Emergency Medical MinutePodcast 1001: Acute Intermediate Risk Pulmonary Embolism | — | pulmonary embolismintermediate risk+6 | — | 3m 17s | ||
| 4/3/26 | medical historysepsis+4 | — | naloxone/narcanHunting for Pancreatitis+20 | — | medical minutessepsis+5 | — | 1h 29m 15s | ||
| 3/30/26 | burn managementfirst aid+3 | Aaron Lessen, MD | Annals of Emergency MedicineBurns | — | burnsfirst-degree burns+4 | — | 2m 39s | ||
| 3/23/26 | internal jugular cathetercentral venous access+3 | Travis Barlock, MD | — | — | internal jugular veincentral venous catheter+5 | — | 2m 44s | ||
| 3/16/26 | overdoseintubation+3 | Aaron Lessen, MD | Annals of Emergency Medicine | — | overdosenaloxone+4 | — | 3m 17s | ||
| 3/9/26 | D-dimerpulmonary embolism+3 | Travis Barlock, MD | Emergency Medical MinuteEgypt J Bronchol+2 | — | D-dimerpulmonary embolism+3 | — | 2m 01s | ||
| 3/2/26 | melatoninsleep+4 | Taylor Lynch MD | FDACell Mol Neurobiol+1 | — | melatoninsleep latency+5 | — | 4m 09s | ||
| 2/24/26 | UTI diagnosisantibiotic treatment+3 | Travis Barlock, MD | JAMA Netw OpenAm Fam Physician | — | UTIdiagnosis+5 | — | 5m 45s | ||
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23 placements across 20 markets.
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23 placements across 20 markets.