1,054 episodes

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.

Emergency Medical Minute Emergency Medical Minute

    • Health & Fitness

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.

    Podcast 912: Narcan (Naloxone)

    Podcast 912: Narcan (Naloxone)

    Contributor: Taylor Lynch, MD
    Educational Pearls:
    Opioid Epidemic- quick facts
    Drug overdoses, primarily driven by opioids, have become the leading cause of accidental death in the U.S. for individuals aged 18-45.
    In 2021, opioids were involved in nearly 75% of all drug overdose deaths
    The rise of synthetic opioids like fentanyl, which is much more potent than heroin or prescription opioids, has played a major role in the increase in overdose deaths
    What is Narcan AKA Naloxone?
    Competitive opioid antagonist. It sits on the receptor but doesn’t activate it.
    When do we give Narcan?
    Respiratory rate less than 8-10 breaths per minute
    Should you check the pupils?
    An opioid overdose classically presents with pinpoint pupils BUT…
    Hypercapnia from bradypnea can normalize the pupils
    Taking other drugs at the same time like cocaine or meth can counteract the pupillary effects
    Basilar stroke could also cause small pupils, so don’t anchor on an opioid overdose
    How does Narcan affect the body?
    Relatively safe even if the patient is not experiencing an opioid overdose. So when in doubt, give the Narcan.
    What if the patient is opioid naive and overdosing?
    Use a large dose given that this patient is unlikely to withdraw
    0.4-2 mg every 3-5 minutes
    What if the patient is a chronic opioid user
    Use a smaller dose such as 0.04-0.4 mg to avoid precipitated withdrawal
    How fast does Narcan work?
    Given intravenously (IV), onset is 1-2 min
    Given intranasal (IN), onset is 3-4 min
    Given intramuscularly (IM), onset is ~6 min
    Duration of action is 60 mins, with a range of 20-90 minutes
    How does that compare to the duration of action of common opioids?
    Heroine lasts 60 min
    Fentanyl lasts 30-60 min, depending on route
    Carfentanyl lasts ~5 hrs
    Methadone lasts 12-24 hrs
    So we really need to be conscious about redosing
    How do you monitor someone treated with Narcan?
    Pay close attention to the end-tidal CO2 to ensure that are ventilating appropriately
    Be cautious with giving O2 as it might mask hypoventilation
    Watch the respiratory rate
    Give Narcan as needed
    Observe for at least 2-4 hours after the last Narcan dose
    Larger the dose, longer the observation period
    Who gets a drip?
    If they have gotten ~3 doses, time to start the drip
    Start at 2/3rds last effective wake-up dose
    Complications
    Flash pulm edema
    0.2-3.6% complication rate
    Might be from the catecholamine surge from abrupt wake-up
    Might also be from large inspiratory effort against a partially closed glottis which creates too much negative pressure
    Treat with BIPAP if awake and intubation if not awake
    Should you give Narcan in cardiac arrest?
    Short answer no. During ACLS you take over breathing for the patient and that is pretty much the only way that Narcan can help
    Just focus on high quality CPR
    References
    https://nida.nih.gov/research-topics/trends-statistics/overdose-death-rates#:~:text=Drug%20overdose%20deaths%20involving%20prescription,of%20deaths%20declined%20to%2014%2C716.
    Elkattawy, S., Alyacoub, R., Ejikeme, C., Noori, M. A. M., & Remolina, C. (2021). Naloxone induced pulmonary edema. Journal of community hospital internal medicine perspectives, 11(1), 139–142. https://doi.org/10.1080/20009666.2020.1854417
    van Lemmen, M., Florian, J., Li, Z., van Velzen, M., van Dorp, E., Niesters, M., Sarton, E., Olofsen, E., van der Schrier, R., Strauss, D. G., & Dahan, A. (2023). Opioid Overdose: Limitations in Naloxone Reversal of Respiratory Depression and Prevention of Cardiac Arrest. Anesthesiology, 139(3), 342–353. https://doi.org/10.1097/ALN.0000000000004622
    Yousefifard, M., Vazirizadeh-Mahabadi, M. H., Neishaboori, A. M., Alavi, S. N. R., Amiri, M., Baratloo, A., & Saberian, P. (2019). Intranasal versus Intramuscular/Intravenous Naloxone for Pre-hospital Opioid Overdose: A Systematic Review and Meta-analysis. Advanced jo

    • 6 min
    Episode 911: Anticholinergic Toxicity

    Episode 911: Anticholinergic Toxicity

    Contributor: Taylor Lynch MD
    Educational Pearls:
    Anticholinergics are found in many medications, including over-the-counter remedies
    Medications include:
    Diphenhydramine
    Tricyclic antidepressants like amitriptyline
    Atropine
    Antipsychotics like olanzapine
    Antispasmodics - dicyclomine
    Jimsonweed
    Muscaria mushrooms
    Mechanism of action involves competitive antagonism of the muscarinic receptor
    Symptomatic presentation is easily remembered via the mnemonic:
    Dry as a bone - anhidrosis due to cholinergic antagonism at sweat glands
    Red as a beet - cutaneous vasodilation leads to skin flushing
    Hot as a hare - anhidrotic hyperthermia
    Blind as a bat - pupillary dilation and ineffective accommodation
    Mad as a hatter - anxiety, agitation, dysarthria, hallucinations, and others
    Clinical management
    ABCs
    Benzodiazepines for supportive care, agitation, and seizures
    Sodium bicarbonate for TCA toxicity due to widened QRS
    Activated charcoal if patient present Temperature monitoring
    Contact poison control with questions
    Physostigmine controversy
    Physostigmine is a reversible cholinesterase inhibitor that can cross the blood-brain barrier so in theory it would be a useful antidote BUT…
    There is a black box warning for asystole and seizures when physostigmine is used this way
    Therefore it is contraindicated in TCA overdoses
    However, it is still indicated in certain anticholinergic overdoses with delirium
    Disposition
    Admission criteria include: symptoms >6 hours, CNS findings, QRS prolongation, hyperthermia, and rhabdomyolysis
    ICU admission criteria include: delirium, dysrhythmias, seizures, coma, or requirement for physostigmine drip
    References
    1. Arens AM, Shah K, Al-Abri S, Olson KR, Kearney T. Safety and effectiveness of physostigmine: a 10-year retrospective review. Clin Toxicol (Phila). 2018;56(2):101-107. doi:10.1080/15563650.2017.1342828
    2. Nguyen TT, Armengol C, Wilhoite G, Cumpston KL, Wills BK. Adverse events from physostigmine: An observational study. Am J Emerg Med. 2018;36(1):141-142. doi:10.1016/j.ajem.2017.07.006
    3. Scharman E, Erdman A, Wax P, et al. Diphenhydramine and dimenhydrinate poisoning: An evidence-based consensus guideline for out-of-hospital management. Clin Toxicol. 2006;44(3):205-223. doi:10.1080/15563650600585920
    4. Shervette RE 3rd, Schydlower M, Lampe RM, Fearnow RG. Jimson "loco" weed abuse in adolescents. Pediatrics. 1979;63(4):520-523.
    5. Woolf AD, Erdman AR, Nelson LS, et al. Tricyclic antidepressant poisoning: An evidence-based consensus guideline for out-of-hospital management. Clin Toxicol. 2007;45(3):203-233. doi:10.1080/15563650701226192
    Summarized by Jorge Chalit, OMSIII | Edited by Jorge Chalit
     

    • 7 min
    Episode 910: Cellulitis Recovery Timeline

    Episode 910: Cellulitis Recovery Timeline

    Contributor: Aaron Lessen, MD
    Educational Pearls:
    How fast does cellulitis recover?
    A recent prospective cohort study took a look at this question.
    The study included 300 adults with cellulitis (excluding those with peri-orbital cellulitis or abscesses) in two emergency departments in Queensland, Australia.
    They collected data from initial and follow-up surveys at 3, 7, and 14 days, and compared clinician and patient assessments at day 14.
    Improvement was fastest between day 0 and day 3, with gradual progress thereafter.
    At day 14, many still had skin redness and swelling, though warmth had often resolved. Clinicians reported higher cure rates than patients (85.8% vs. 52.8%).
    Conclusion:
    Cellulitis symptoms improve quickly at first but continue to linger for many patients.
    Patients and doctors often have different views on when cellulitis is fully cured.
    How should we counsel patients?
    Even on antibiotics, the margins of the cellulitis may continue to spread a small amount.
    Skin warmth should be the first symptom to go away.
    It takes time to get better. Only about 50% of patients believed their cellulitis was cured at 2 weeks.
    References
    Nightingale, R. S., Etheridge, N., Sweeny, A. L., Smyth, G., Dace, W., Pellatt, R. A. F., Snelling, P. J., Yadav, K., & Keijzers, G. (2024). Cellulitis in the Emergency Department: A prospective cohort study with patient-centred follow-up. Emergency medicine Australasia : EMA, 10.1111/1742-6723.14401. Advance online publication. https://doi.org/10.1111/1742-6723.14401
    Summarized by Jeffrey Olson MS2 | Edited by Meg Joyce & Jorge Chalit, OMSIII

    • 1 min
    Episode 909: Prehospital Blood Pressure Management in Suspected Stroke

    Episode 909: Prehospital Blood Pressure Management in Suspected Stroke

    Contributor: Aaron Lessen MD
    Educational Pearls:
    A recent study assessed EMS treatment of high blood pressure in the field
    2404 patients randomized to prehospital treatment (1205)  vs. usual care (1199)
    Included patients with prehospital BP greater than 150 mm Hg
    The treatment arm’s BP goal was 130-140 mm Hg
    The primary efficacy outcome was functional status 90 days out
    Stroke was confirmed by imaging upon hospital arrival
    On arrival, the mean SBP of the treatment arm was 159 mm Hg compared with 170 mm Hg in the usual care group
    No significant difference in functional outcomes between the treatment group and the usual care group (Common Odds Ratio of 1.00, 95% CI = 0.87-1.15)
    Post-imaging analysis revealed 46.5% of the undifferentiated patients had a hemorrhagic stroke
    Prehospital reduction in BP did reduce the odds of poor functional outcome in hemorrhagic stroke patients alone (Common Odds Ratio 0.75, 95% CI 0.60-0.92)
    Those with ischemic stroke had increased odds of poor functional outcome (Common Odds Ratio 1.30, 95% CI 1.06-1.60)
    Bottom line: it is challenging to identify the stroke type in the prehospital setting and therefore not necessarily helpful to treat the blood pressure
    References
    1. Ren X, Zhang C, Xu P, et al. Intensive Ambulance-Delivered Blood- Pressure Reduction in Hyperacute Stroke. New England Journal of Medicine. 2024;390(20):1862-1872. doi:10.1056/NEJMoa2314741
    Summarized by Jorge Chalit, OMSIII | Edited by Meg Joyce & Jorge Chalit
     

    • 2 min
    Episode 908: Sympathomimetic Drugs

    Episode 908: Sympathomimetic Drugs

    Contributor: Taylor Lynch MD
    Educational Pearls:
    Overview: Sympathomimetic drugs mimic the fight or flight response, affecting monoamines such as dopamine, norepinephrine, and epinephrine Limited therapeutic use, often abused. Types: Amphetamines: Methamphetamine, Adderall, Ritalin, Vyvanse MDMA (Ecstasy) Cocaine (Both hydrochloride salt & free based crack cocaine) Theophylline (Asthma treatment) Ephedrine (For low blood pressure) BZP, Oxymetazoline (Afrin), Pseudoephedrine (Sudafed) MAO Inhibitors (treatment-resistant depression) Mechanisms: Act on adrenergic and dopaminergic receptors. Cocaine blocks dopamine and serotonin reuptake. Methamphetamines increase stimulatory neurotransmitter release MAO Inhibitors prevent neurotransmitter breakdown. Symptoms: Agitation, tachycardia, hypertension, hyperactive bowel sounds, diuresis, hyperthermia. Severe cases: Angina, seizures, cardiovascular collapse. Diagnosis: Clinical examination and history. Differentiate from anticholinergic toxidrome by diaphoresis and hyperactive bowel sounds. Tests: EKG, cardiac biomarkers, chest X-ray, blood gas, BMP, CK, coagulation studies, U-tox screen. Treatment: Stabilize ABCs, IV hydration, temperature monitoring, benzodiazepines. Avoid beta-blockers due to unopposed alpha agonism. Whole bowel irrigation for body packers; surgical removal if packets rupture. IV hydration for high CK levels. Observation period often necessary. Recap: Mimic sympathetic nervous system. Key symptoms: Diaphoresis, hyperactive bowel sounds. Treatment: Supportive care, benzodiazepines. Use poison control as a resource. References:
    Costa VM, Grazziotin Rossato Grando L, Milandri E, Nardi J, Teixeira P, Mladěnka P, Remião F. Natural Sympathomimetic Drugs: From Pharmacology to Toxicology. Biomolecules. 2022;12(12):1793. doi:10.3390/biom12121793
    Kolecki P. Sympathomimetic Toxicity From Emergency Medicine. Medscape. Updated March 11, 2024. https://emedicine.medscape.com/article/818583-overview
    Williams RH, Erickson T, Broussard LA. Evaluating Sympathomimetic Intoxication in an Emergency Setting. Lab Med. 2000;31(9):497-508. https://doi.org/10.1309/WVX1-6FPV-E2LC-B6YG
    Summarized by Steven Fujaros | Edited by Jorge Chalit, OMSIII
     

    • 7 min
    Episode 907: Wide-Complex Tachycardia

    Episode 907: Wide-Complex Tachycardia

    Contributor: Travis Barlock MD
    Educational Pearls:
    Wide-complex tachycardia is defined as a heart rate > 100 BPM with a QRS width > 120 milliseconds
    Wide-complex tachycardia of supraventricular origin is known as SVT with aberrancy
    Aberrancy is due to bundle branch blocks
    Mostly benign
    Treated with adenosine or diltiazem
    Wide-complex tachycardia of ventricular origin is also known as VTach
    Originates from ventricular myocytes, which are poor inherent pacemakers
    Dangerous rhythm that can lead to death
    Treated with amiodarone or lidocaine
    80% of wide-complex tachycardias are VTach
    90% likelihood for patients with a history of coronary artery disease
    In assessing a wide-complex tachycardia, it is best to treat it as a presumed ventricular tachycardia
    Treating SVT with amiodarone or lidocaine does no harm 
    However, treating VTach with adenosine or diltiazem may worsen the condition
    References
    1. Littmann L, Olson EG, Gibbs MA. Initial evaluation and management of wide-complex tachycardia: A simplified and practical approach. Am J Emerg Med. 2019;37(7):1340-1345. doi:https://doi.org/10.1016/j.ajem.2019.04.027
    2. Viskin S, Chorin E, Viskin D, Hochstadt A, Schwartz AL, Rosso R. Polymorphic Ventricular Tachycardia: Terminology, Mechanism, Diagnosis, and Emergency Therapy. Circulation. 2021;144(10):823-839. doi:10.1161/CIRCULATIONAHA.121.055783
    3. Williams SE, O’Neill M, Kotadia ID. Supraventricular tachycardia: An overview of diagnosis and management. Clin Med J R Coll Physicians London. 2020;20(1):43-47. doi:10.7861/clinmed.cme.20.1.3
    Summarized by Jorge Chalit, OMSIII | Edited by Meg Joyce & Jorge Chalit

    • 3 min

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