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Mortality And Morbidity Conference Dr. Meenakshi Aggarwal PGY2 Emory University Family Medicine
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AGENDAAGENDA Case Review Discussion Take Home Points
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CASE HISTORY C/C: Sudden loss of consciousness HPI: 32 Y/o WM brought in by EMS due to sudden loss of consciousness and found to be having V-Fib cardiac arrest. PMH: None PSH: None SHx: Smoker 1 PPD x 15yrs, occasional alcohol, no drugs. Works as a car mechanic.
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History Contd : Meds: None Allergies: Latex FHx: H/o seizures in paternal grandfather and 2 nephews.
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Physical Examination VS: T: 98F, HR: 89, BP: 117/63, SPo2: 99% on vent O/E: Intubated HEENT: Pupils sluggishly reactive B/L Chest: Coarse breath sounds CVS: RRR, No M/G/R Abd: Soft, NT/ND Neuro: Unresponsive. DTR 2+ Ext: No C/C/E Skin: No rash
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LABSLABS CBC: H&H: 15.4/43.8, WBC’s: 6.8, Plat: 298,000 Chem: Na 143, K 3.4, BUN 16, Cr 1.1, BG 134, Ca 8.8 LFT’s: AST 134, ALT 99, Alk PO4 113 S.alcohol: 0.105 UDS: Neg CE: CK 231, CKMB 2, troponin 0.04 U/A: Normal
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Sinus Tachycardia
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Management in the ER Narcaine Lidocaine drip Bicarb Ativan Versed drip
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BUT……BUT…… Pts urine looks GREEN. IS THE PATIENT HAVING ETHYLENE GLYCOL POISONING??? Pt treated with Fomepizole and sent to the ICU.
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Miscellaneous Labs TSH: 3.08 Ethyl Alcohol: 0.105 Isopropyl Alcohol: Pending Methanol: Pending Ethylene Glycol: Pending
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ST segment elevation in leads V1-V6 and reciprocal depression in the inferior leads.
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Is this patient having MI???
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Management in the ICU Lidocaine drip d/ced and amiodarone drip started. Pt was given loading dose of lovenox and EKG repeated. ASA given through nasogastric tube and CE’s sent Cardiologist was called Lopressor I/V x3 given
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Patient needs to be transported through air ambulance BUT crew not available. Wait….. Wait…. Finally, after 2 hrs, patient transported by road ambulance at 6 am in the morning.
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ST segment elevation in V1-V3 with RBBB
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Brugada Syndrome Disorder characterized by ST segment elevation in leads V1 through V3 on EKG RBBB EKG abnormalities may not be evident until unmasked by flecainide or procainamide infusion (antiarrythmic drugs) or augmented by beta blockers.
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Brugada Syndrome Structurally normal heart Sudden death or syncope Presentation characteristic of ventricular fibrillation or ventricular tachycardia No prodromal symptoms
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Typical electrocardiogram of Brugada syndrome. Note the pattern resembling a right bundle branch block, the P-R prolongation and the ST elevation in leads V1-V3.
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Etiology Autosomal Dominant Mutations in gene SCN5A that encodes for the sodium channels in the heart. Other genetic mutations also found
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Schematic of SCN5A. Some mutations are associated with combined phenotypes. α = Subunit
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Drugs that can induce BS like EKG pattern Na channel blockers: Class IC drugs (flecainide,encainide) Class IA drugs ( procainamide) Lithium Ca channel blockers Beta blockers TCA (amitriptyline, nortriptyline) SSRI’s ( Fluoxetine) Cocaine Intoxication Alcohol intoxication
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FeatureType 1Type 2Type 3 J wave amplitude > 2 mm T waveNegativePositive or biphasic Positive ST-T configuration Coved typeSaddle back ST segment (terminal portion) Gradually descending Elevated > 1mm Elevated < 1 mm Types Of EKG Patterns in BS
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Types of EKG patterns in BS:
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Treatment ICD ( Implantable cardioverter - defibrillator) Pharmacotherapy: No proven drugs
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Conclusion NN ever compare your own urine with the patient’s urine…..
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Take home points Syndrome of ST segment elevation in V1-V3, RBBB and sudden death Genetically determined Sudden death can only be prevented by ICD’s
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QUESTIONS?
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