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...
Contributor: Travis Barlock, MD Educational Pearls: What is Hoover’s sign used to identify? This physical exam maneuver differentiates between organic vs. functional (previously known as psychogenic) leg weakness. Organic causes include disease processes such as stroke, MS, spinal cord compression, guillain-barre, ALS, and sciatica, among others In Functional Neurologic Disorder, the dysfunction is in brain signaling, and treatment relies on more of a psychiatric approach How is Hoover's Sign performed? Place your hand under the heel of the unaffected leg and ask the patient to attempt to lift the paralyzed leg. If the paralysis is due to an organic cause, then you should feel the unaffected leg push down. This is due to the crossed-extensor reflex mechanism, an unconscious motor control function mediated by the corticospinal tract. If you don’t feel the opposite heel push down, that is a positive Hoover’s Sign. How sensitive/specific is it? An unblinded cohort study in patients with suspected stroke found a sensitivity of 63% and a specificity of 100% Fun Fact There’s also a pulmonary Hoover’s sign, named after the same doctor, Charles Franklin Hoover, which refers to paradoxical inward movement of the lower ribs during inspiration due to diaphragmatic flattening in COPD. References McWhirter L, Stone J, Sandercock P, Whiteley W. Hoover's sign for the diagnosis of functional weakness: a prospective unblinded cohort study in patients with suspected stroke. J Psychosom Res. 2011 Dec;71(6):384-6. doi: 10.1016/j.jpsychores.2011.09.003. Epub 2011 Oct 6. PMID: 22118379. Stone J, Aybek S. Functional limb weakness and paralysis. Handb Clin Neurol. 2016;139:213-228. doi: 10.1016/B978-0-12-801772-2.00018-7. PMID: 27719840. Summarized by Jeffrey Olson, MS3 | Edited by Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/
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Episode 948: CYP Inducers and Inhibitors
Contributor: Jorge Chalit-Hernandez, OMS3 Educational Pearls: CYP enzymes are responsible for the metabolism of many medications, drugs, and other substances CYP3A4 is responsible for the majority Other common ones include CYP2D6 (antidepressants), CYP2E1 (alcohol), and CYP1A2 (cigarettes) CYP inducers lead to reduced concentrations of a particular medication CYP inhibitors effectively increase concentrations of certain medications in the body Examples of CYP inducers Phenobarbital Rifampin Cigarettes St. John’s Wort Examples of CYP inhibitors -azole antifungals like itraconazole and ketoconazole Bactrim (trimethoprim-sulfamethoxazole) Ritonavir (found in Paxlovid) Grapefruit juice Clinical relevance Drug-drug interactions happen frequently and often go unrecognized or underrecognized in patients with significant polypharmacy A study conducted on patients receiving Bactrim and other antibiotics found increased rates of anticoagulation in patients receiving Bactrim Currently, Paxlovid is prescribed to patients with COVID-19, many of whom have multiple comorbidities and are on multiple medications Paxlovid contains ritonavir, a powerful CYP inhibitor that can increase concentrations of many other medications A complete list of clinically relevant CYP inhibitors can be found on the FDA website: https://www.fda.gov/drugs/drug-interactions-labeling/drug-development-and-drug-interactions-table-substrates-inhibitors-and-inducers References Glasheen JJ, Fugit RV, Prochazka AV. The risk of overanticoagulation with antibiotic use in outpatients on stable warfarin regimens. J Gen Intern Med. 2005;20(7):653-656. doi:10.1111/j.1525-1497.2005.0136.x Lynch T, Price A. The effect of cytochrome P450 metabolism on drug response, interactions, and adverse effects. Am Fam Physician. 2007;76(3):391-396. PAXLOVID™. Drug interactions. PAXLOVIDHCP. Accessed March 16, 2025. https://www.paxlovidhcp.com/drug-interactions Summarized & Edited by Jorge Chalit, OMS3 Donate: https://emergencymedicalminute.org/donate/
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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/
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.