Emergency Medical Minute

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**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 is recorded in a real emergency department, by the emergency physician or clinical pharmacist on duty – the ER is our studio and everything is live.

Latest Episodes:

Podcast 1027: Oculocardiac Reflex Oct 19, 2026

Show notes

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

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Podcast 1026: Esophageal Balloon Tamponade Devices Oct 17, 2026

Show notes

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.

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Podcast 1025: Post intubation Sedation Oct 12, 2026

Show notes

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

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Podcast 1024: Caffeine Toxicity Oct 05, 2026

Show notes

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

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Podcast 1023: Torsades de pointes Sep 28, 2026

Show notes

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

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Podcast 1022: Emergent Dialysis Sep 21, 2026

Show notes

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

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Podcast 1021: Pulmonary Edema From Naloxone Administration Sep 14, 2026

Show notes

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

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Podcast 1020: Benign Paroxysmal Positional Vertigo (BPPV) Sep 07, 2026

Show notes

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

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Podcast 1019: Trauma Blunt Cardiovascular Injuries (BCVI) Aug 31, 2026

Show notes

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

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Podcast 1018: Occult Ventricular Fibrillation on Echocardiography Aug 24, 2026

Show notes

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

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