Emergency Medical Minute

• Episode 947: Hypercapnia

  Educational Pearls: Physiologic stimulation of ventilation occurs through changes in levels of: Arterial carbon dioxide (PaCO2) Arterial oxygen (PaO2) Hypercapnia is an elevated level of CO2 in the blood - this primarily drives ventilation Hypoxia is a decreased level of O2 in the body’s tissues - the backup drive for ventilation Patients at risk of hypercapnia should maintain an O2 saturation between 88-92% Normal O2 saturation is 95-100% In patients who chronically retain CO2, their main drive for ventilation becomes hypoxia An audit was performed of SpO2 observations of all patients with a target range of 88–92% at a single hospital over a four-year period This found that excessive oxygen administration was more common than insufficient oxygen and is associated with an increased risk of harm Individuals at risk of hypercapnia include but are not limited to patients with COPD, hypoventilation syndrome, or altered mental status References Homayoun Kazemi, Douglas C. Johnson, Respiration, Editor(s): V.S. Ramachandran, Encyclopedia of the Human Brain, Academic Press, 2002, Pages 209-216, ISBN 9780122272103, https://doi.org/10.1016/B0-12-227210-2/00302-2. O'Driscoll BR, Bakerly ND. Are we giving too much oxygen to patients at risk of hypercapnia? Real world data from a large teaching hospital. Respir Med. 2025 Mar;238:107965. doi: 10.1016/j.rmed.2025.107965. Epub 2025 Jan 30. PMID: 39892771. Summarized by Meg Joyce, MS1 | Edited by Meg Joyce & Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/  

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• Episode 946: Time to Defibrillation

  Contributor: Aaron Lessen, MD Educational Pearls: Quick background info Cardiac arrest is when the heart stops pumping blood for any reason. This is different from a heart attack in which the heart is still working but the muscle itself is starting to die. One cause of cardiac arrest is when the electrical signals are very disrupted in the heart and start following chaotic patterns such as Ventricular tachycardia (VTach) and Ventricular fibrillation (VFib) One of the only ways to save a person whose heart is in VFib or VTach is to jolt the heart with electricity and terminate the dangerous arrhythmia. A recent study in the Netherlands looked at how important the time delay is from when cardiac arrest is first identified to when a defibrillation shock from an Automated External Defibrillator (AED) is actually given. Their main take-away: each minute defibrillation is delayed drops the survival rate by 6%! These findings reinforce the importance of rapid AED deployment and early defibrillation strategies in prehospital cardiac arrest response. References Stieglis, R., Verkaik, B. J., Tan, H. L., Koster, R. W., van Schuppen, H., & van der Werf, C. (2025). Association Between Delay to First Shock and Successful First-Shock Ventricular Fibrillation Termination in Patients With Witnessed Out-of-Hospital Cardiac Arrest. Circulation, 151(3), 235–244. https://doi.org/10.1161/CIRCULATIONAHA.124.069834 Summarized by Jeffrey Olson, MS3 | Edited by Meg Joyce, MS1 & Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/  

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• Episode 945: Ketorolac vs. Ibuprofen

  Contributor: Ricky Dhaliwal, MD Educational Pearls:  Ketorolac and ibuprofen are NSAIDs with equivalent efficacy for pain in the emergency department Oral ibuprofen provides the same relief as intramuscular ketorolac IM ketorolac is associated with the adverse effect of a painful injection IM ketorolac is slightly faster in onset but not significant Studies have assessed the two medications in head-to-head randomized-controlled trials and found no significant difference in pain scores IM ketorolac takes longer to administer and has a higher cost Ketorolac dosing Commonly given in 10 mg, 15 mg, and 30 mg doses However, higher doses are associated with more adverse effects Gastrointestinal upset, nausea, and bleeding risk Studies have demonstrated equal efficacy in pain reduction with lower doses References Motov S, Yasavolian M, Likourezos A, et al. Comparison of Intravenous Ketorolac at Three Single-Dose Regimens for Treating Acute Pain in the Emergency Department: A Randomized Controlled Trial. Ann Emerg Med. 2017;70(2):177-184. doi:10.1016/j.annemergmed.2016.10.014 Neighbor ML, Puntillo KA. Intramuscular ketorolac vs oral ibuprofen in emergency department patients with acute pain. Acad Emerg Med. 1998;5(2):118-122. doi:10.1111/j.1553-2712.1998.tb02595.x Summarized & Edited by Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/  

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• Episode 944: Colchicine Overdose

  Contributor: Aaron Lessen, MD Educational Pearls: Colchicine is most commonly used for the prevention and treatment of gout There is research investigating the anti-inflammatory and cardioprotective effects of colchicine  This drug has a narrow therapeutic index: a small margin between effective dose and toxic dose Colchicine overdoses can be unintentional or intentional and are associated with poor outcomes Phase 1: 10 - 24 hours after ingestion Patient looks well but may have mild symptoms mimicking gastroenteritis Phase 2: 24 hours - 7 days after ingestion Multiple organ dysfunction syndrome (MODS) Phase 3: recovery is usually within a few weeks of ingestion Treatment for colchicine overdose Treat early and aggressively Gastrointestinal decontamination with activated charcoal and orogastric lavage  Dialysis and ECMO for MODS treatment References Finkelstein Y, Aks SE, Hutson JR, Juurlink DN, Nguyen P, Dubnov-Raz G, Pollak U, Koren G, Bentur Y. Colchicine poisoning: the dark side of an ancient drug. Clin Toxicol (Phila). 2010 Jun;48(5):407-14. doi: 10.3109/15563650.2010.495348. PMID: 20586571. Gasparyan AY, Ayvazyan L, Yessirkepov M, Kitas GD. Colchicine as an anti-inflammatory and cardioprotective agent. Expert Opin Drug Metab Toxicol. 2015;11(11):1781-94. doi: 10.1517/17425255.2015.1076391. Epub 2015 Aug 4. PMID: 26239119. Summarized by Meg Joyce, MS1 | Edited by Meg Joyce & Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/  

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• Episode 943: Portal Vein Thrombosis

  Contributor: Travis Barlock, MD Educational Pearls: What is Portal Vein Thrombosis? The formation of a blood clot within the portal vein, which carries blood from the gastrointestinal tract, pancreas, and spleen to the liver Not only can this cause problems downstream in the liver, but the backup of venous blood can cause ischemia in the bowels How does it present? Similar to acute mesenteric ischemia: Sudden onset of abdominal pain, nausea, vomiting, and fever How is it diagnosed? Abdominal CT or MRI with contrast What causes it? Cirrhosis Coagulopathy (Factor V Leiden mutation, Prothrombin gene mutation, Antiphospholipid syndrome, Protein C, protein S, antithrombin III deficiency, etc.) Oral Contraceptive Pills (OCPs) Cancer such as hepatocellular carcinoma How is it treated? Aggressive fluid resuscitation Antibiotics. Be sure to cover enteric gram-negative bacteria and anaerobes Heparin, same dosing as a bolus for a DVT Endovascular treatment, such as a thrombectomy with IR Surgical evaluation if there has been tissue death in the mesentery References Hilscher, M. B., Wysokinski, W. E., Andrews, J. C., Simonetto, D. A., Law, R. J., & Kamath, P. S. (2024). Portal Vein Thrombosis in the Setting of Cirrhosis: Evaluation and Management Strategies. Gastroenterology, 167(4), 664–672. https://doi.org/10.1053/j.gastro.2024.05.017 Intagliata, N. M., Caldwell, S. H., & Tripodi, A. (2019). Diagnosis, Development, and Treatment of Portal Vein Thrombosis in Patients With and Without Cirrhosis. Gastroenterology, 156(6), 1582–1599.e1. https://doi.org/10.1053/j.gastro.2019.01.265 Ju, C., Li, X., Gadani, S., Kapoor, B., & Partovi, S. (2022). Portal Vein Thrombosis: Diagnosis and Endovascular Management. Pfortaderthrombose: Diagnose und endovaskuläres Management. RoFo : Fortschritte auf dem Gebiete der Rontgenstrahlen und der Nuklearmedizin, 194(2), 169–180. https://doi.org/10.1055/a-1642-0990 Summarized by Jeffrey Olson MS3 | Edited by Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/  

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