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We review threatened abortion and the complexities in its care. Hosts: Stacey Frisch, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Threatened_Abortion.mp3 Download One Comment Tags: OBGYN Show Notes Background * Defined as vaginal bleeding during early pregnancy (before 20 weeks) with a closed cervical os, no passage of fetal tissue, and IUP on ultrasound * Occurs in 20-25% of all pregnancies. Initial Assessment and Management * Priority is to assess patient stability, establish good IV access, FAST may be helpful in identifying some ruptured ectopics early * Broad differential diagnosis is crucial to avoid mistaking conditions like ectopic pregnancy for other emergencies. * Importance of a detailed history and physical examination. Diagnostic Approach * Essential tests include HCG level, urinalysis, and possibly CBC + blood type/Rh status. * Rhogam’s use is well-supported in second and third trimester bleeding; however, data is less robust for first trimester bleeding in preventing sensitization * Importance of interpreting b-HCG with caution and understanding HCG discriminatory zones. * Use of ultrasound imaging, both bedside and formal, to assess the pregnancy’s status. Patient Counseling and Management * Open and honest communication about the prognosis of threatened abortion. * Addressing psychosocial aspects, including dispelling guilt and myths, and screening for intimate partner violence and mental health issues. * Recommendations against bedrest and certain activities * Lack of evidence supporting restrictions on sexual activity. * Standard pregnancy guidelines: avoiding smoking, alcohol, drug use, and starting prenatal vitamins. Follow-up and Precautions * Adopting a wait-and-see approach for stable patients, with scheduled follow-ups for ultrasounds and beta-HCG tests. * Educating patients on critical warning signs that require immediate medical attention. * Emphasizing the importance of returning to the hospital if experiencing significant bleeding or other severe symptoms. Take Home Points * Threatened Abortion is defined as Experiencing abdominal pain and/or vaginal bleeding during early pregnancy (before 20 weeks), characterized by a closed cervical os and no expulsion of fetal tissue. In these cases, it is important to assess patient stability promptly. * Keep your differential broad in these cases. The evaluation will in most cases involve a combination of labs and ultrasound imaging.  * Understand that the Rhogam certainly has a role in second and third trimester vaginal bleeding in the Rh-negative patient, and that there is a dearth of good data on its role in the first trimester – it will ultimately be a decision that is made by you, OBGYN, and the patient. 

We review a general approach to syncope in children. Hosts: Brian Gilberti, MD Ellen Duncan, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Syncope_in_Children.mp3 Download Leave a Comment Tags: Cardiology, Pediatrics Show Notes * Initial Evaluation and Management: * Similar initial workup for children and adults: checking glucose levels for hypoglycemia and conducting an EKG. * The history and physical exam are crucial. * Dextrose Administration in Children: * Explanation of the ‘rule of 50s’ for determining the appropriate dextrose solution and dosage for children. * ECG Analysis: * Importance of ECG in diagnosing dysrhythmias like long QT syndrome, Brugada syndrome, catecholamine polymorphic V tach, ARVD, ALCAPA, and Wolff-Parkinson-White syndrome. * Younger children’s dependency on heart rate for cardiac output and the risk of arrhythmias in kids with congenital heart disease. Condition Characteristic ECG Findings Congenital/Acquired Long QT Syndrome (LQTS) Prolonged QT interval Congenital/Acquired Wolff-Parkinson-White Syndrome (WPW) Short PR interval, Delta wave Congenital Brugada Syndrome ST elevation in V1-V3, Right bundle branch block Congenital Atrioventricular Block (AV Block) PR interval prolongation (1st degree), Missing QRS complexes (2nd & 3rd degree) Congenital/Acquired Supraventricular Tachycardia (SVT) Narrow QRS complexes, Absence of P waves, Tachycardia Congenital/Acquired Ventricular Tachycardia Wide QRS complexes, Tachycardia Congenital/Acquired Arrhythmogenic Right Ventricular Dysplasia (ARVD/C) Epsilon waves, V1-V3 T wave inversions, Right bundle branch block Congenital Hypertrophic Cardiomyopathy (HCM) Left ventricular hypertrophy, Deep Q waves Congenital Pulmonary Hypertension Right ventricular hypertrophy, Right axis deviation Acquired Athlete’s Heart Sinus bradycardia, Voltage criteria for left ventricular hypertrophy Acquired Catecholaminergic Polymorphic VT (CPVT) Bidirectional or polymorphic VT, typically normal at rest Congenital Anomalous Origin of Left Coronary Artery from Pulmonary Artery (ALCAPA) May be normal, signs of ischemia or infarction in severe cases Congenital * History Taking: * Key aspects include asking about syncope with exertion, syncope after being startled, and syncope after pain or emotional stress.

We go over the treatment of rapid atrial fibrillation (afib with RVR). Hosts: Brian Gilberti, MD Jonathan Kobles, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Rapid_Atrial_Fibrillation.mp3 Download One Comment Tags: Cardiology Show Notes Understanding AF with RVR Categories General AF with RVR: Definition and basic understanding. Rapid AF with Pre-excitation: Characteristics and complications. Chronic AF in Critical Illness: Identification and special considerations. Stability Assessment in AF with RVR ACLS Protocols: Distinction between unstable and stable patients. Unstable Patients: Immediate need for synchronized cardioversion, standard dose at 200 J for adults. Stable Patients: Rate vs. rhythm control strategies, consideration of underlying etiology. Limitations in Chronic AF: Challenges in patients with AF secondary to critical illness. ACLS Guidelines and ECG Findings Tachycardia with a Pulse Approach: Initial assessment guidelines. ECG Interpretation: Irregularly Irregular Rhythm: Absence of discernible P waves. Ventricular Rate: Typically over 100 bpm. QRS Complexes: Usually narrow, alterations in the presence of bundle branch block or ventricular rate-related aberrancy. Identifying Pre-Excitation Syndromes: Signs of shortened PR interval and slurred QRS, indication of Wolff-Parkinson-White Syndrome. AF with Pre-Excitation (WPW Syndrome) Risk Assessment: Dangers of using AV nodal blockers (BB/CCB, digoxin, adenosine). Alternative Management: Utilization of procainamide or amiodarone for stable patients, synchronized electrical cardioversion for unstable patients. Treatment Approaches for AF Types General Rapid AF: First Line Agents: Metoprolol vs. Diltiazem. Metoprolol Considerations: Dosing (5 mg every 10-15 minutes, max 15 mg), benefits in CAD and HF, limitations in asthma/COPD patients. Diltiazem Advantages: Faster action, suitability in asthma/COPD, typical dosing (0.25 mg/kg initial, followed by 0.35 mg/kg if needed). Critically Ill Patients: Tailoring treatment to underlying pathology, avoiding typical AF pharmacologic treatments. Systematic Evaluation of Tachycardia Causes (TACHIES Mnemonic) Thyrotoxicosis, Alcohol withdrawal, Cardiac issues, Hemorrhage, Intervals (WPW), Embolus, Sepsis. Application of the mnemonic for a comprehensive approach to differential diagnosis. Ultrasound in Diagnostic Assessment Application in Undiagnosed Tachycardia: Identifying EF, pericardial effusion, valvular pathology, and signs of pulmonary embolism. Fluid Status Evaluation: Use of ultrasound for assessing b-lines in lung scans. Management of Chronic AF with HD Instability

We discuss Electrical Storm (VT storm) and how to care for the very irritable heart. Hosts: Brian Gilberti, MD Reed Colling, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Electrical_Storm.mp3 Download Leave a Comment Tags: Cardiology Show Notes Background/Overview of VT: Definition: What makes it a storm  Three or more sustained episodes of VF, VT, or appropriate ICD shocks in a 24-hour period Pathophysiology: Understanding the origin and mechanism Sympathetic drive/adrenergic surge Underlying pathology: Sodium channelopathies, infiltrative disease like cardiac sarcoidosis, etc. RF’s / trigger / population (reversible cause in ~25% of patients) MI Electrolyte Derangements (emphasis on potassium and magnesium) New/worsening heart failure Catecholamine Surge Drugs (stimulants, cocaine, amphetamines, etc) QT Prolongation Thyrotoxicosis Clinical Presentation: Symptoms of VT: spectrum of symptoms – from palpitations to syncope to cardiac arrest Differentiating VT from other potential ER presentations. Diagnostics in ER: Electrocardiogram (ECG): Recognizing VT patterns. Monomorphic vs polymorphic (Torsades) may change management Wide QRS Fusion best Capture beats Concordance  AV-dissociation Lab tests: Potassium, magnesium, troponins, TFTs, etc. Acute Management in the ER: Hemodynamically stable vs. unstable V Unstable = cardioversion Sedation Catecholamine surge should be considered  No ideal agent  Etomidate or propofol can be considered  Ketamine may worsen irritability  Pharmacological treatments: Amiodarone Class III antiarrhythmic  Most studied in VT storm  First line Beta Blockers Propranolol B1 and B2 activity  Non-pharmacological approaches: Immediate synchronized cardioversion IABP / ECMO considered for HD unstable patient Cath lab if ischemic etiology suspected  Stellate Ganglion Block Take Home Points Definition: VT Storm is commonly defined as three or more sustained episodes of ventricular fibrillation, ventricular tachycardia, or appropriate ICD shocks within a 24-hour period. Varied Presentation: Patients may experience a range of symptoms from palpitations to severe hemodynamic instability. ECG and Diagnosis: Initial ECG may not show VT; continuous cardiac monitoring or device interrogation may be required for diagnosis. VT Identification: Look for wide QRS, rate over 100, fusion beats, capture beats, and AV dissociation to identify VT. Management in Hemodynamic Instability: Cardiovert if the...

We revisit the topic of Hyperkelamia to update our prior episode from 2015 (pre-Lokelma) Hosts: Brian Gilberti, MD Jonathan Kobles, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Hyperkalemia.mp3 Download 2 Comments Tags: Renal Colic Show Notes Introduction * Background Physiology: Normal range and the significance of deviations (>5.5 mEq/L) Epidemiology: Prevalence of hyperkalemia in the ER ESRD missed HD → ECG, monitor Causes / Risk Factors Causes Kidney Dysfunction, Medications,  Cellular Destruction,  Endocrine Causes, Pseudohyperkalemia High-Risk Medications: Antibiotics: Bactrim, antifungals Calcineurin inhibitors Beta-blockers ACE/ARB K+ Sparing diuretics NSAIDs Digoxin SUX – high risks in neuromuscular disease Lab errors, hemolysis in samples VBG vs Chem accuracy  When to repeat a hemolyzed sample  2023 study: Of the 145 children with hemolyzed hyperkalemia, 142 (97.9%) had a normal repeat potassium level. Three children (2.1%) had true hyperkalemia: one had known chronic renal failure and was referred to the ED due to concern for electrolyte abnormalities; the other 2 patients had diabetic ketoacidosis (DKA). Clinical Presentation / eval  Symptomatic vs. Asymptomatic: “First symptom of hyperkalemia is death”  If severe, ascending muscle weakness → paralysis  Point at which patients experience symptoms depends on chronicity >7 mEq/L if chronic and can be lower if acute Hyperkalemia can be a cause of non-specific GI symptoms EKG Changes: ECG findings may be the first marker the ER doc gets that something is wrong Typical changes:  Peaked T-waves, shortened QT Lengthening of PR interval and QRS duration  Bradycardia / Junctional rhythm Hyperkalemia can produce bradycardia without other ECG findings Ones associated with VT/VF/code, death in one study: QRS widening (RR = 4.74),

We go over the essential and complex topic of vasopressors in the ED. Hosts: Brian Gilberti, MD Catherine Jamin, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Vasopressors.mp3 Download Leave a Comment Tags: Critical Care Show Notes Introduction * Host: Brian Gilberti, MD * Guest: Catherine Jamin, MD * Associate professor of Emergency Medicine at NYU Langone Health * Vice Chair of Operations * Triple-boarded in Emergency Medicine, Internal Medicine, and Critical Care Medicine * Topic: Vasopressors: Essential agents for supporting critically ill patients in the ED What Are Vasopressors and When to Use Them * Two primary mechanisms to increase blood pressure: * Increasing systemic vascular resistance via vasoconstriction * Increasing cardiac output via augmenting inotropy and chronotropy * Indicators for vasopressor use: * MAP 65 * Max Dose: No strict limit but usually add a 2nd pressor at 15-20 mcg/min * Situational Preference: First-line for most cases of shock (septic, undifferentiated, hypovolemic, cardiogenic) * Pros: Can be infused peripherally via large bore IV Vasopressin * Mechanism: Activates V1a receptors causing vasoconstriction * Dose: Fixed, non-titratable dose of 0.04 units/min * Situational Preference: Second-line in septic shock * Concerns: Potential for peripheral ischemia Phenylephrine * Mechanism: Stimulates alpha-1 receptors causing vasoconstriction * Starting Dose: 100 mcg/min, titrate to MAP >65 * Situational Preference: High cardiac output states, tachyarrhythmias, peri-intubation * Concerns: Increases afterload, can worsen low cardiac output states Epinephrine * Mechanism: Stimulates alpha-1, beta-1 and beta-2 receptors * Starting Dose: 5-10 mcg/min, titrate to MAP >65 * Situational Preference: Anaphylactic shock, septic cardiomyopathy * Limitations: Can induce tachycardia, may elevate lactate levels Escalation Strategy in Refractory Shock * Norepinephrine -> Vasopressin (with stress dose steroids) -> Epinephrine * Consider POCUS, lactate, central venous saturation, and acid-base status

We discuss the diagnosis and management of septic arthritis in the pediatric population. Hosts: Brian Gilberti, MD Ellen Duncan, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Septic_Joint_in_Children.mp3 Download 2 Comments Tags: Infectious Diseases, Pediatrics Show Notes General Pain in joint for pediatric patient has a broad differential, including transient synovitis and septic arthritis Transient synovitis, also known as toxic synovitis, is a common condition affecting kids aged 3-10 and often occurs after a viral infection. It is typically self-limiting and not considered a serious condition. Septic arthritis is an infection in the joint space, typically affecting only one joint. It is often difficult to diagnose due to the fact that many patients, particularly under the age of 3, may not be able to localize their pain to a specific joint. Workup Diagnostic work-up for septic arthritis begins with blood work, which includes a complete blood count (CBC), erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and blood cultures. Lyme disease studies may also be necessary since Lyme disease can cause joint pain. Patients with transient synovitis typically have mild elevation in inflammatory markers, while those with septic arthritis usually show a significant elevation. Imaging studies, including X-rays, ultrasound to evaluate for a joint effusion, and MRI to assess for associated osteomyelitis, are also part of the diagnostic approach. The Kocher criteria, developed specifically for septic arthritis of the hip, are a useful tool for clinical decision-making. The criteria include fever above 38.5 C, inability to bear weight, ESR above 40, and a white blood cell count above 12,000. 1 criterion met = 3% probability of septic arthritis 2 criteria met = 40% probability of septic arthritis 3 criteria met = 93% probability of septic arthritis 4 criteria met = 99+% probability of septic arthritis   If septic arthritis is suspected, orthopedics should be consulted immediately. Joint fluid aspiration is necessary for diagnosis and should not be delayed. The fluid should be sent for cell count, gram stain, glucose, culture, and PCR if available. Septic arthritis is most commonly caused by bacterial infections, with Staph aureus being the most common organism. In school-age children, other bacteria such as Strep pyogenes, Strep pneumoniae, and Haemophilus influenzae should also be considered. In preschool-aged children, K. kingae is also considered. In older children and neonates, the range of potential bacteria varies. Management

A quick primer on hypocalcemia in the ED. Hosts: Joseph Offenbacher, MD Audrey Bree Tse, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/hypocalcemia.mp3 Download 4 Comments Tags: calcium, Critical Care, Endocrine Show Notes Swami’s CoreEM Post Hypocalcemia Repletion: * IV calcium supplementation with 100-300 mg Ca2+ raises serum Ca2+ by 0.5 – 1.5 mEq * For acute but mild symptomatic hypocalcemia: 200-1000mg calcium chloride IV or 1-2g IV calcium gluconate over 2 hours *  For severe hypocalcemia: 1g calcium chloride IV or 1-2g IV calcium gluconate IV over 10 minutes repeated q 60 min until symptoms resolve References: * Cooper MS, Gittoes NJ. Diagnosis and management of hypocalcaemia. BMJ 2008; 336:1298. * ​​Desai TK, Carlson RW, Geheb MA. Prevalence and clinical implications of hypocalcemia in acutely ill patients in a medical intensive care setting. Am J Med 1988; 84:209. * Goltzman, D. Diagnostic approach to hypocalcemia. UpToDate. UpToDate; Jul 17, 2020. Accessed April 29, 2022. https://www.uptodate.com/contents/plantar-fasciitis * Kelly A, Levine MA. Hypocalcemia in the critically ill patient. J Intensive Care Med 2013; 28:166. * Pfenning CL, Slovis CM: Electrolyte Disorders; in Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 8. St. Louis, Mosby, Inc., 2014, (Ch) 125: p 1636-53. * Swaminathan, A. (2016, January 27). Hypocalcemia. CoreEM. Retrieved April 29, 2022, from https://coreem.net/core/hypocalcemia/ * Vantour L, Goltzman D. Regulation of calcium homeostasis. In: rimer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, 9th ed, Bilezikian JP (Ed), Wiley-Blackwell, Hoboken, NJ 2018. p.163. Read More

How and when to reverse anticoagulation in the bleeding EM patient. Hosts: Joe Offenbacher, MD Audrey Bree Tse, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/AC_reversal.mp3 Download 3 Comments Tags: Anticoagulation, Critical Care, Resuscitation Show Notes Coagulation Cascade:   Algorithm for Anticoagulated Bleeding Patient in the ED:     Indications for Anticoagulation Reversal:   References:  Baugh CW, Levine M, Cornutt D, et al. Anticoagulant Reversal Strategies in the Emergency Department Setting: Recommendations of a Multidisciplinary Expert Panel. Ann Emerg Med. 2020;76(4):470-485. doi:10.1016/j.annemergmed.2019.09.001 Eikelboom JW, Quinlan DJ, van Ryn J, Weitz JI. Idarucizumab: The Antidote for Reversal of Dabigatran. Circulation. 2015 Dec 22;132(25):2412-22. doi: 10.1161/CIRCULATIONAHA.115.019628. PMID: 26700008. Fariborz Farsad B, Golpira R, Najafi H, et al. Comparison between Prothrombin Complex Concentrate (PCC) and Fresh Frozen Plasma (FFP) for the Urgent Reversal of Warfarin in Patients with Mechanical Heart Valves in a Tertiary Care Cardiac Center. Iran J Pharm Res. 2015;14(3):877-885. Fariborz Farsad B, Golpira R, Najafi H, et al. Comparison between Prothrombin Complex Concentrate (PCC) and Fresh Frozen Plasma (FFP) for the Urgent Reversal of Warfarin in Patients with Mechanical Heart Valves in a Tertiary Care Cardiac Center. Iran J Pharm Res. 2015;14(3):877-885. Palta S, Saroa R, Palta A. Overview of the coagulation system. Indian J Anaesth. 2014;58(5):515-523. doi:10.4103/0019-5049.144643 Siegal DM, Curnutte JT, Connolly SJ, Lu G, Conley PB, Wiens BL, Mathur VS, Castillo J, Bronson MD, Leeds JM, Mar FA, Gold A, Crowther MA. Andexanet Alfa for the Reversal of Factor Xa Inhibitor Activity. N Engl J Med. 2015 Dec 17;373(25):2413-24. doi: 10.1056/NEJMoa1510991. Epub 2015 Nov 11. PMID: 26559317. Read More

A primer on this airway/ ID/ ENT emergency. Hosts: Joe Offenbacher MD, A Bree Tse, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/ludwigs_2.mp3 Download 2 Comments Tags: Airway, ENT, Infectious Diseases Show Notes References: Botha A, Jacobs F, Postma C. Retrospective analysis of etiology and comorbid diseases associated with Ludwig’s Angina. Ann Maxillofac Surg 2015; 5:168. Boscolo-Rizzo P, Da Mosto MC. Submandibular space infection: a potentially lethal infection. Int J Infect Dis 2009; 13:327. Brook I. Microbiology and principles of antimicrobial therapy for head and neck infections. Infect Dis Clin North Am. 2007 Jun;21(2):355-91, vi. doi: 10.1016/j.idc.2007.03.014. PMID: 17561074. Chong W, Hijazi M, Abdalrazig M, Patil N. Respect the Floor of the Mouth. J Emerg Med. 2020 Jul;59(1):e27-e29. doi: 10.1016/j.jemermed.2020.04.015. Epub 2020 May 19. PMID: 32439254. http://www.emdocs.net/ludwigs-angina-2/ Mohamad I, Narayanan MS. “Double Tongue” Appearance in Ludwig’s Angina. N Engl J Med 2019; 381:163. Saifeldeen K, Evans R. Ludwig’s angina. Emerg Med J. 2004 Mar;21(2):242-3. doi: 10.1136/emj.2003.012336. PMID: 14988363; PMCID: PMC1726306. Wolfe MM, Davis JW, Parks SN. Is surgical airway necessary for airway management in deep neck infections and Ludwig angina? J Crit Care. 2011 Feb;26(1):11-4. doi: 10.1016/j.jcrc.2010.02.016. PMID: 20537506. Read More

A quick overview of pneumothorax for the EM physician: the what, why, diagnosis, and treatment. Hosts: Joe Offenbacher, MD Audrey Tse, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Pneumothorax_CoreEM_podcast.mp3 Download One Comment Tags: #pneumothorax #FOAMed Show Notes Shownotes: CoreEM Pulmonary Ultrasound Post References: Bense L, Lewander R, Eklund G, et al. Nonsmoking, non-alpha 1-antitrypsin deficiency-induced emphysema in nonsmokers with healed spontaneous pneumothorax, identified by computed tomography of the lungs. Chest 1993; 103:433. Bense L, Wiman LG, Hedenstierna G. Onset of symptoms in spontaneous pneumothorax: correlations to physical activity. Eur J Respir Dis 1987; 71:181. Brown SGA, Ball EL, Perrin K, Asha SE, Braithwaite I, Egerton-Warburton D, Jones PG, Keijzers G, Kinnear FB, Kwan BCH, Lam KV, Lee YCG, Nowitz M, Read CA, Simpson G, Smith JA, Summers QA, Weatherall M, Beasley R; PSP Investigators. Conservative versus Interventional Treatment for Spontaneous Pneumothorax. N Engl J Med. 2020 Jan 30;382(5):405-415. doi: 10.1056/NEJMoa1910775. PMID: 31995686. Chardoli M, Hasan-Ghaliaee T, Akbari H, Rahimi-Movaghar V. Accuracy of chest radiography versus chest computed tomography in hemodynamically stable patients with blunt chest trauma. Chin J Traumatol 2013; 16:351. Chan KK, Joo DA, McRae AD, et al. Chest ultrasonography versus supine chest radiography for diagnosis of pneumothorax in trauma patients in the emergency department. Cochrane Database Syst Rev 2020; 7:CD013031. Ebrahimi A, Yousefifard M, Mohammad Kazemi H, et al. Diagnostic Accuracy of Chest Ultrasonography versus Chest Radiography for Identification of Pneumothorax: A Systematic Review and Meta-Analysis. Tanaffos 2014; 13:29. Gobbel Jr WG, Rhea Jr WG, Nelson IA, Daniel RA. Spontaneous pneumothorax. J Thorac Cardiovasc Surg 1963; 46:331. Lesur O, Delorme N, Fromaget JM, et al. Computed tomography in the etiologic assessment of idiopathic spontaneous pneumothorax. Chest 1990; 98:341. Lichtenstein DA, Mezière G, Lascols N, et al. Ultrasound diagnosis of occult pneumothorax. Crit Care Med 2005; 33:1231. Melton LJ 3rd, Hepper NG, Offord KP. Influence of height on the risk of spontaneous pneumothorax. Mayo Clin Proc 1981; 56:678. Ohata M, Suzuki H. Pathogenesis of spontaneous pneumothorax. With special reference to the ultrastructure of emphysematous bullae. Chest 1980; 77:771. Sahn SA, Heffner JE. Spontaneous pneumothorax. N Engl J Med 2000; 342:868.   Read More

An interesting back story on this must-not-miss EKG finding in the ED! Hosts: Joseph Offenbacher, MD Audrey Bree Tse, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/CoreEM_Wellens.mp3 Download One Comment Tags: #FOAMed, #wellens, Cardiology, EKG, STEMI Show Notes Hosts: Joe Offenbacher MD, Audrey Bree Tse MD EKG Findings in de Zwaan C, Bär FW, Wellens HJ. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J. 1982 Apr;103(4 Pt 2):730-6. doi: 10.1016/0002-8703(82)90480-x. PMID: 6121481. Table 1 in de Zwaan C, Bär FW, Wellens HJ. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J. 1982 Apr;103(4 Pt 2):730-6. doi: 10.1016/0002-8703(82)90480-x. PMID: 6121481. REFERENCES: de Zwaan C, Bär FW, Wellens HJ. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J. 1982 Apr;103(4 Pt 2):730-6. doi: 10.1016/0002-8703(82)90480-x. PMID: 6121481. Lee, M., & Chen, C. (2015). Myocardial Bridging: An Up-to-Date Review. Journal of Invasive Cardiology, 27(11), 521–528.  https://lifeinthefastlane.com/ecg-library/wellens-syndrome/ Lin AN, Lin S, Gokhroo R, Misra D. Cocaine-induced pseudo-Wellens’ syndrome: a Wellens’ phenocopy. BMJ Case Rep. 2017 Dec 14;2017:bcr2017222835. doi: 10.1136/bcr-2017-222835. PMID: 29246935; PMCID: PMC5753703. Rhinehardt, J., Brady, W. J., Perron, A. D., & Mattu, A. (2002). Electrocardiographic manifestations of Wellens’ syndrome. The American Journal of Emergency Medicine, 20(7), 638–643. https://doi.org/10.1053/ajem.2002.34800 Tandy, TK; Bottomy DP; Lewis JG (March 1999). “Wellens’ syndrome”. Annals of Emergency Medicine. 33 (3): 347–351. PMID 10036351. doi:10.1016/S0196-0644(99)70373-2. (via Wikipedia) Read More