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

Contributor: Aaron Lessen MD

Educational Pearls:

The case:

• A gentleman came in from a nursing home with symptoms concerning for sepsis. He was hypotensive, hypoxic, febrile, and mentally altered.

• His past medical history included previous strokes which had left him with deficits for which he required a feeding tube.

• Initial workup included some point of care labs which revealed a sodium of 165 mEq/L (normal range 135-145)

Hypernatremia

• What causes it?

• Dehydration, from insufficient fluid intake. This might happen in individuals who cannot drink water independently, such as infants, elderly, or disabled people, as was the case for this patient.

• Other causes of dehydration/hypernatremia include excessive sweating; diabetes insipidus; diuretic use; kidney dysfunction; and severe burns which can lead to fluid loss through the damaged skin.

• How do you correct it?

• Need to correct slowly, not more than 10 to 12 meq/L in 24 hours

• Can do normal saline (0.9%) or half saline (0.45%) and D5, at 150-200 mL per hour.

• Check the sodium frequently (every 2-3 hours)

• Will likely need ICU-level monitoring

• What happens if you correct it too quickly?

• Cerebral edema

• Seizures

Bonus fact: Correction of hyponatremia too quickly causes osmotic demyelination syndrome (ODS).

References

1. Chauhan, K., Pattharanitima, P., Patel, N., Duffy, A., Saha, A., Chaudhary, K., Debnath, N., Van Vleck, T., Chan, L., Nadkarni, G. N., & Coca, S. G. (2019). Rate of Correction of Hypernatremia and Health Outcomes in Critically Ill Patients. Clinical journal of the American Society of Nephrology : CJASN, 14(5), 656–663. https://doi.org/10.2215/CJN.10640918

2. Lindner, G., & Funk, G. C. (2013). Hypernatremia in critically ill patients. Journal of critical care, 28(2), 216.e11–216.e2.16E20. https://doi.org/10.1016/j.jcrc.2012.05.001

3. Muhsin, S. A., & Mount, D. B. (2016). Diagnosis and treatment of hypernatremia. Best practice & research. Clinical endocrinology & metabolism, 30(2), 189–203. https://doi.org/10.1016/j.beem.2016.02.014

Summarized by Jeffrey Olson MS2 | Edited by Meg Joyce & Jorge Chalit, OMSIII

Contributor: Aaron Lessem MD

Educational Pearls:

• Oseltamivir (Tamiflu) is an antiviral medication used commonly to treat influenza

• Trials show that the medication reduces the duration of illness by less than 1 day (~16 hours in one systematic review)

• Benefit only occurs if taken within 48 hours of symptom onset

• Must be taken for 5 days

• A 2024 meta-analysis reviewed 15 randomized-controlled trials for the risk of hospitalization

• No reduction in hospitalizations with oseltamivir in patients over the age of 12

• No difference in high-risk patients over the age of 65 or those with comorbidities

• The authors note that the confidence interval in these populations is wide, indicating a need for subsequent studies in high-risk populations

• Oseltamivir is associated with adverse effects including nausea, vomiting, and neurologic symptoms

• The risk of adverse effects may outweigh the benefits of a small reduction in the duration of illness

References

1. Hanula R, Bortolussi-Courval É, Mendel A, Ward BJ, Lee TC, McDonald EG. Evaluation of Oseltamivir Used to Prevent Hospitalization in Outpatients with Influenza: A Systematic Review and Meta-Analysis. JAMA Intern Med. 2024;184(1):18-27. doi:10.1001/jamainternmed.2023.0699

2. Jefferson T, Jones M, Doshi P, Spencer EA, Onakpoya I, Heneghan CJ. Oseltamivir for influenza in adults and children: Systematic review of clinical study reports and summary of regulatory comments. BMJ. 2014;348(April):1-18. doi:10.1136/bmj.g2545

Summarized by Jorge Chalit, OMSII | Edited by Meg Joyce & Jorge Chalit

Contributor: Aaron Lessen MD

Educational Pearls:

Epinephrine is essential in the treatment of anaphylaxis, but is epinephrine dangerous from a cardiovascular perspective?

A 2024 study in the Journal of the American College of Emergency Physicians Open sought to answer this question.

Methods:

• Retrospective observational study at a Tennessee quaternary care academic ED that analyzed ED visits from 2017 to 2021 involving anaphylaxis treated with IM epinephrine.

• The primary outcome was cardiotoxicity

Results:

• Out of 338 patients, 16 (4.7%) experienced cardiotoxicity. Events included ischemic EKG changes (2.4%), elevated troponin (1.8%), atrial arrhythmias (1.5%), ventricular arrhythmia (0.3%), and depressed ejection fraction (0.3%).

• Affected patients were older, had more comorbidities, and often received multiple epinephrine doses.

Bottom line:

• All adults presenting with anaphylaxis should be rapidly treated with epinephrine but monitored closely for cardiotoxicity, especially in patients with a history of hypertension and those who receive multiple doses.

These results are supported by a 2017 study that found that 9% (4/44) of older patients who received epinephrine for anaphylaxis had cardiovascular complications.

References

1. Kawano, T., Scheuermeyer, F. X., Stenstrom, R., Rowe, B. H., Grafstein, E., & Grunau, B. (2017). Epinephrine use in older patients with anaphylaxis: Clinical outcomes and cardiovascular complications. Resuscitation, 112, 53–58. https://doi.org/10.1016/j.resuscitation.2016.12.020

2. Pauw, E. K., Stubblefield, W. B., Wrenn, J. O., Brown, S. K., Cosse, M. S., Curry, Z. S., Darcy, T. P., James, T. E., Koetter, P. E., Nicholson, C. E., Parisi, F. N., Shepherd, L. G., Soppet, S. L., Stocker, M. D., Walston, B. M., Self, W. H., Han, J. H., & Ward, M. J. (2024). Frequency of cardiotoxicity following intramuscular administration of epinephrine in emergency department patients with anaphylaxis. Journal of the American College of Emergency Physicians open, 5(1), e13095. https://doi.org/10.1002/emp2.13095

Summarized by Jeffrey Olson MS2 | Edited by Meg Joyce & Jorge Chalit OMS II

Contributor: Aaron Lessen MD

Educational Pearls:

• Opioid overdoses that are reversed with naloxone (Narcan), a mu-opioid antagonist, can precipitate acute withdrawal in some patients

• Treatment of opioid use disorder with buprenorphine can also precipitate withdrawal

• Opioid withdrawal symptoms include nausea, vomiting, diarrhea, and agitation

• Buprenorphine works as a partial agonist at mu-opioid receptors, which may alleviate withdrawal symptoms

• The preferred dose of buprenorphine is 16 mg

• Treatment of buprenorphine-induced opioid withdrawal is additional buprenorphine

• Adjunctive treatments may be used for other opioid withdrawal symptoms

• Nausea with ondansetron

• Diarrhea with loperamide

• Agitation with hydroxyzine

References

1. Quattlebaum THN, Kiyokawa M, Murata KA. A case of buprenorphine-precipitated withdrawal managed with high-dose buprenorphine. Fam Pract. 2022;39(2):292-294. doi:10.1093/fampra/cmab073

2. Spadaro A, Long B, Koyfman A, Perrone J. Buprenorphine precipitated opioid withdrawal: Prevention and management in the ED setting. Am J Emerg Med. 2022;58:22-26. doi:10.1016/j.ajem.2022.05.013

Summarized by Jorge Chalit, OMSII | Edited by Meg Joyce & Jorge Chalit

Contributor: Travis Barlock MD

Educational Pearls:

How do you differentiate between compensated and decompensated cirrhosis?

Use the acronym VIBE to look for signs of being decompensated.

• V-Volume

• Cirrhosis can cause volume overload through a variety of mechanisms such as by increasing pressure in the portal vein system and the decreased production of albumin.

• Look for pulmonary edema (dyspnea, orthopnea, wheezing/crackles, coughing up frothy pink sputum, etc.) or a tense abdomen.

• I-Infection

• The ascitic fluid can become infected with bacteria, a complication called Spontaneous Bacterial Peritonitis (SBP).

• Look for abdominal pain, fever, hypotension, and tachycardia. Diagnosis is made with ascitic fluid cell analyses (polymorphonuclear neutrophils >250/mm3)

• B-Bleeding

• Another consequence of increased portal pressure is that blood backs up into smaller blood vessels, including those in the esophagus.

• Over time, this increased pressure can result in the development of dilated, fragile veins called esophageal varices, which are prone to bleeding.

• Look for hematemesis, melena, lightheadedness, and pale skin.

• E-Encephalopathy

• A failing liver also does not clear toxins which can affect the brain.

• Look for asterixis (flapping motion of the hands when you tell the patient to hold their hands up like they are going to stop a bus)

Other complications to look out for.

• Hepatorenal syndrome

• Hepatopulmonary syndrome

References

1. Engelmann, C., Clària, J., Szabo, G., Bosch, J., & Bernardi, M. (2021). Pathophysiology of decompensated cirrhosis: Portal hypertension, circulatory dysfunction, inflammation, metabolism and mitochondrial dysfunction. Journal of hepatology, 75 Suppl 1(Suppl 1), S49–S66. https://doi.org/10.1016/j.jhep.2021.01.002

2. Enomoto, H., Inoue, S., Matsuhisa, A., & Nishiguchi, S. (2014). Diagnosis of spontaneous bacterial peritonitis and an in situ hybridization approach to detect an "unidentified" pathogen. International journal of hepatology, 2014, 634617. https://doi.org/10.1155/2014/634617

3. Mansour, D., & McPherson, S. (2018). Management of decompensated cirrhosis. Clinical medicine (London, England), 18(Suppl 2), s60–s65. https://doi.org/10.7861/clinmedicine.18-2-s60

Summarized by Jeffrey Olson MS2 | Edited by Meg Joyce & Jorge Chalit, OMS II

Contributor: Aaron Lessen MD

Educational Pearls:

• Lorazepam (Ativan) is dosed at 0.1 mg/kg up to a maximum of 4 mg in status epilepticus

• Some ED protocols only give 2 mg initially

• The maximum recommended dose of levetiracetam (Keppra) is 60 mg/kg or 4.5 g

• In one retrospective study, only 50% of patients received the correct dose of lorazepam

• For levetiracetam, it was only 35% of patients

• Underdosing leads to complications

• Higher rates of intubations

• More likely to progress to refractory status epilepticus

References

1. Cetnarowski A, Cunningham B, Mullen C, Fowler M. Evaluation of intravenous lorazepam dosing strategies and the incidence of refractory status epilepticus. Epilepsy Res. 2023;190(November 2022):107067. doi:10.1016/j.eplepsyres.2022.107067

2. Sathe AG, Tillman H, Coles LD, et al. Underdosing of Benzodiazepines in Patients With Status Epilepticus Enrolled in Established Status Epilepticus Treatment Trial. Acad Emerg Med. 2019;26(8):940-943. doi:10.1111/acem.13811

Summarized by Jorge Chalit, OMSII | Edited by Meg Joyce & Jorge Chalit

Contributor: Travis Barlock MD

Educational Pearls:

Ketamine is an NMDA receptor antagonist with a wide variety of uses in the emergency department. To dose ketamine remember the numbers 0.3, 1, and 3.

Pain dose

• For acute pain relief administer 0.3 mg/kg of ketamine IV over 10-20 minutes (max of 30 mg).

• Note: There is evidence that a lower dose of 0.1-0.15 mg/kg can be just as effective.

Dissociative dose

• To use ketamine as an induction agent for intubation or for procedural sedation administer 1 mg/kg IV over 1-2 minutes.

IM for acute agitation

• If a patient is out of control and a danger to themselves or others, administer 3 mg/kg intramuscularly (max 500 mg).

• If you are giving IM ketamine it has to be in the concentrated 100 mg/ml vial.

Additional pearls

• Pushing ketamine too quickly can cause laryngospasm.

• Between .3 and 1 mg/kg is known as the recreational dose. You want to avoid this range because this is where ketamine starts to pick up its dissociative effects and can cause unpleasant and intense hallucinations. This is colloquially known as being in the "k-hole".

References

1. Gao, M., Rejaei, D., & Liu, H. (2016). Ketamine use in current clinical practice. Acta pharmacologica Sinica, 37(7), 865–872. https://doi.org/10.1038/aps.2016.5

2. Lin, J., Figuerado, Y., Montgomery, A., Lee, J., Cannis, M., Norton, V. C., Calvo, R., & Sikand, H. (2021). Efficacy of ketamine for initial control of acute agitation in the emergency department: A randomized study. The American journal of emergency medicine, 44, 306–311. https://doi.org/10.1016/j.ajem.2020.04.013

3. Stirling, J., & McCoy, L. (2010). Quantifying the psychological effects of ketamine: from euphoria to the k-Hole. Substance use & misuse, 45(14), 2428–2443. https://doi.org/10.3109/10826081003793912

Summarized by Jeffrey Olson MS2 | Edited by Jorge Chalit, OMS II

Contributor: Travis Barlock MD

Educational Pearls:

• Thrombolytic therapy (tPA or TNK) is often used in the ED for strokes

• Use of anticoagulants with INR > 1.7 or PT >15

• Warfarin will reliably increase the INR

• Current use of Direct thrombin inhibitor or Factor Xa inhibitor

• aPTT/PT/INR are insufficient to assess the degree of anticoagulant effect of Factor Xa inhibitors like apixaban (Eliquis) and rivaroxaban (Xarelto)

• Intracranial or intraspinal surgery in the last 3 months

• Intracranial neoplasms or arteriovenous malformations also increase the risk of bleeding

• Current intracranial or subarachnoid hemorrhage

• History of intracranial hemorrhage from thrombolytic therapy also contraindicates tPA/TNK

• Recent (within 21 days) or active gastrointestinal bleed

• Hypertension

• BP >185 systolic or >110 diastolic

• Administer labetalol before thrombolytics to lower blood pressure

• Timing of symptoms

• Onset > 4.5 hours contraindicates tPA

• Platelet count

• BGL

• Potential alternative explanation for stroke-like symptoms obviating need for thrombolytics

References

1. Fugate JE, Rabinstein AA. Absolute and Relative Contraindications to IV rt-PA for Acute Ischemic Stroke. The Neurohospitalist. 2015;5(3):110-121. doi:10.1177/1941874415578532

2. Powers WJ, Rabinstein AA, Ackerson T, et al. Guidelines for the Early Management of Patients with Acute Ischemic Stroke: 2019 Update to the 2018 Guidelines for the Early Management of Acute Ischemic Stroke a Guideline for Healthcare Professionals from the American Heart Association/American Stroke Association. Vol 50.; 2019. doi:10.1161/STR.0000000000000211

Summarized by Jorge Chalit, OMSII | Edited by Jorge Chalit

Contributor: Ricky Dhaliwal, MD

Educational Pearls:

• Takotsubo cardiomyopathy, also known as "broken heart syndrome," is a temporary heart condition that can mimic the symptoms of a heart attack, including troponin elevations and mimic STEMI on ECG.

• The exact cause is not fully understood, but it is often triggered by severe emotional or physical stress. The stress can lead to a surge of catecholamines which affects the heart (multivessel spasm/paralysed myocardium).

• The name "Takotsubo" comes from the Japanese term for a type of octopus trap, as the left ventricle takes on a distinctive shape resembling this trap during systole. The LV is dilated and part of the wall becomes akenetic. These changes can be seen on ultrasound.

• The population most at risk for Takotsubo are post-menopausal women.

• Coronary angiography is one of the only ways to differentiate Takotsubo from other acute coronary syndromes.

• Most people with Takotsubo cardiomyopathy recover fully.

References

1. Amin, H. Z., Amin, L. Z., & Pradipta, A. (2020). Takotsubo Cardiomyopathy: A Brief Review. Journal of medicine and life, 13(1), 3–7. https://doi.org/10.25122/jml-2018-0067

2. Bossone, E., Savarese, G., Ferrara, F., Citro, R., Mosca, S., Musella, F., Limongelli, G., Manfredini, R., Cittadini, A., & Perrone Filardi, P. (2013). Takotsubo cardiomyopathy: overview. Heart failure clinics, 9(2), 249–x. https://doi.org/10.1016/j.hfc.2012.12.015

3. Dawson D. K. (2018). Acute stress-induced (takotsubo) cardiomyopathy. Heart (British Cardiac Society), 104(2), 96–102. https://doi.org/10.1136/heartjnl-2017-311579

4. Kida, K., Akashi, Y. J., Fazio, G., & Novo, S. (2010). Takotsubo cardiomyopathy. Current pharmaceutical design, 16(26), 2910–2917. https://doi.org/10.2174/138161210793176509

Summarized by Jeffrey Olson MS2 | Edited by Jorge Chalit, OMSII