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MEDiscuss • Cardiovascular diseases • What is the difference between NSTEMI and STEMI? Streptokinase in NSTEMI?


  1. #11
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    Thank you for the reply Shashikiran.

    If one does decide to use streptokinase as a last, life-saving option, how should it be administered? I assume the usual method of diluting in 100mls fluid won't work well if circulation is impaired by cardiac arrest.

    Regards,
    keno

  2. #12
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    Again, as there are no recommendations available, it is difficult to give a correct answer.

    The attachments with articles on the use of thrombolytics during CPR and may be of help.
    Attached Files Attached Files

  3. #13
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    Thanks!

    These posts were a big help to me, thanks!
    Shashikiran likes this.

  4. #14
    Jen
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    ACS

    hello! first of all thank you all so much for your contribution here, helped me alot!
    so just to confirm that i picked up the right things..


    Management of STEMI,
    - Morphine (to reduce myocardial stress)
    - Supplemental Oxygen (to increase myocardial tissue perfusion)
    - Aspirin (anti-platelet agent)
    - IV Streptokinase/ rTPA (Fibronolytics to lyse the clots)


    Management of NSTEMI and UA,
    - PTCA (clot might not have formed, so stenting can re-establish blood flow)
    - Morphine (to reduce myocardial stress)
    - Supplemental Oxygen (to increase myocardial tissue perfusion)
    - IV GTN/Nitroglycerin (vasodilation)
    - LMWHeparin (anti-coagulant)
    - Aspirin (anti-platelet agent)


    and one more thing, skip IV GTN in STEMI?


    thank you all so much for your help!
    Last edited by Jen; June 6th, 2010 at 10:17 AM.

  5. #15
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    hello,
    @shashikiran, excellent discussion, thank you!
    @medstudent: apart from what shashikiran has excellently elaborated, another reason why thrombolytics(streptokinase)
    is not used in nstemi is probably as follows:

    Lets go back to the pathophysiology of nstemi. Atheromatous plaque ruptures, leading to a thrombus is the basic pathophysiology
    of ACS. Now in NSTEMI, what is proposed is that components of the ruptured plaque and/or platelet aggregates get embolised(away
    from the primary site of rupture and thrombus) causing microemboli, leading to microinfarcts.
    Hence, management of NSTEMI includes STABILITY of the plaque. Thrombolytic therapy can lead to more microinfarcts, hence is
    contraindicated as it can cause more damage.
    hope this was helpful,

    regards,
    rnrm.
    Shashikiran likes this.

  6. #16
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    STEMI is ST-segment elevation and elevation MI NSTEMI non-ST myocardial infarction. Because STEMI is caused by the sudden thrombotic occlusion (formation of a blood clot) of a coronary artery, the mainstay of treatment is thrombolytic therapy (treatment to dissolve the clot). NSTEMI caused by unstable plaque with platelet aggregation.

  7. #17
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    STEMI is when there is a transmural infartion of the myocardium - which just means that the entire thickness of the myocardium has undergone necrosis - resulting in ST elevation. While NSTEMI is when there is a partial dynamic block to coronary arteries (non-occlusive thrombus). There will be no ST elevation or Q waves on ECG, as transmural infarction is not seen. This is the main difference between STEMI and NSTEMI.

 

 
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