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 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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Podcast 1017: CPR Hand Placement Aug 17, 2026

Show notes

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

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Podcast 1016: Hypokalemia Aug 10, 2026

Show notes

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

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Podcast 1015: Calcium in Hyperkalemia Aug 03, 2026

Show notes

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

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Podcast 1014: Eating and Drinking on Shift Jul 27, 2026

Show notes

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

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