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  • Diagnosis then Treatment...?



    42yr old male presents for emergent Lap Appendectomy and you get this great history from previous records.

    Has a history of previous pulseless arrest a year ago. Recovery occurred after basic cardiopulmonary resuscitation, before the arrival of the paramedic ambulance crew. A further episode of monitored VFib in the ambulance required a single 200 J cardioversion. He had no history of angina or previous syncope and there was no family history of sudden death. At the hospital the patient had a 12‐lead ECG showing a partial right bundle branch block with a ‘coved’ pattern of ST elevation in leads V1 to V3 with no elevation in cardiac enzymes.

    I'd like to first talk about the patient's history and see if someone can come up with a diagnosis from the data I gave. Like to see Students work this out with differentials and lets just start a discussion and then we can move into treatment and anesthetic management of the case.
    This article was originally published in forum thread: Diagnosis then Treatment...? started by PaSSiNG GaS View original post
    Comments 2 Comments
    1. PaSSiNG GaS's Avatar
      PaSSiNG GaS -
      - It's an autosomal dominant disease with a molecular defect of gene SCN5A encoding the cardiac sodium channel mapped to 3p21-p23. Familial occurrence has been described with an autosomal dominant pattern of inheritance.

      - More prevalent in Asian population from previous studies

      - Seven genotypes of BrS have been characterized, including muta- tions in cardiac sodium (types 1, 2, 5, and 7), potassium (type 6), and calcium (types 3 and 4) channels.8 Type 1 BrS, sec- ondary to mutations in the SCN5A-encoded Nav1.5 sodium channel a-subunit, is the most common genetic subtype accounting for about 20-30% of BrS. The type 1 Brugada ECG pattern is the most specific ECG pattern for BrS. Type 1 is characterized by a coved-type ST segment elevation of at least 2 mm in the right precordial leads associated with a complete or incomplete right bundle branch block followed by a negative T wave.

      - Could be the cause of 20-60% of idiopathic Vfib

      - Major sign on EKG is incomplete or complete RBBB with ST elevation in V1-V3

      - Class I anti arrhythmic drugs can induce ST segment elevation (Procainamide)

      - Muscarinic and alpha agonists can cause increased ST elevation

      - Basically any drug that can decrease the action potential and has the possibility of working on cardiac sodium channels can induce the ST changes.

      - One main drug that may help decrease the ST elevation is Isoproterenol due to the increase in Ca current and things like phenylephrine may worsen it.

      Below are two articles I found on the subject. I posted this thread because I do a good amount of EP stuff and this is easily something many people can see even if they don't go up to the cath lab or EP.

      Attachment 4108

      Attachment 4109
    1. ckh23's Avatar
      ckh23 -
      This was a good information. Thanks for sharing.