Emergency Medical Minute

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

1. 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

2. 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

3. 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

4. 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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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

1. 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.

2. 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/

3. 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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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

1. 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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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:

1. 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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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:

1. 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

2. DailyMed - NALOXONE HYDROCHLORIDE injection, solution. https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=201fdedf-1736-4e52-9d7d-de14292547fd

3. Boyer EW. Management of Opioid Analgesic Overdose. New England Journal of Medicine. 2012;367(2):146-155. doi:10.1056/NEJMra1202561

4. 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

5. 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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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

1. 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

2. 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

3. 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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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

1. 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.

2. Biffl WL, et al. Screening for and treatment of blunt cerebrovascular injuries: Western Trauma Association critical decisions algorithm. J Trauma. 2009.

3. Brommeland T, et al. Best practice guidelines for blunt cerebrovascular injury. Scand J Trauma Resusc Emerg Med. 2018.

4. 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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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

1. 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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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:

1. 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.

2. 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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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:

1. 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

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

3. 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

4. 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

5. Han EJ, Park JS. Lethal Arrhythmia Induced by Licorice. J Korean Med Sci. 2023;38(12):e107. doi:10.3346/jkms.2023.38.e107

6. 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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