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This has been termed a “STEMI equivalent” and included in STEMI guidelines, suggesting this patient should receive dual anti-platelets, heparin and immediate cath lab activation–or thrombolysis in centres where cath lab is not available. His response: “subendocardial ischemia. Anything more on history?
Computer read: "Non-specific ST abnormality, consider anterior subendocardial ischemia" There are very poor R-waves in V1-V4 suggesting old anterior MI. Firstly, subendocardial ischemia does not localize on 12-Lead ECG. But the real question at hand is: Are these precordial ST-depressions a result of subendocardial ischemia?
Here is the prehospital ECG, with pain: Hyperacute anterolateral STEMI The medics had activated the cath lab and the patient went for angiogram and had a 95% stenotic LAD with TIMI-3 flow. For those who depend on echocardiogram to confirm the ECG findings of ischemia, this should be sobering. Type B waves are deeper and symmetric.
A second 12 Lead ECG was recorded: This is a testament to the dynamic nature of coronary thrombosis and thrombolysis. it has been subsequently deemed a STEMI-equivalent. The patient verbalized spontaneous improvement just before 324mg ASA administration. But the lesion is still active!
Smith15, and PERFECT Study Author Group 1 Hennepin County Medical Center, 2 Minneapolis Medical Research Foundation, 3 Background : The Smith-modified Sgarbossa criteria (MSC) are frequently recommended for diagnosing acute coronary occlusion (ACO; STEMI-equivalent) in the setting of ventricular paced rhythm (VPR).
cm diameter in the apex The presence of thrombus led the clinicians to state that this was a "late presentation STEMI." It does take some time for thrombus to form, but the EKG and the troponin profile show that this was NOT a late presentation STEMI. LV Thrombus , 1.5 0 0 1 95 544 MMRF 4 1 638 14.0 Methods: Vermeer et al.
I am going to code this as an acute STEMI as he had transient ST elevation which started to evolve in the emergency department but I think this is most appropriately termed STEMI." Is this Acute Ischemia? When is it anterior STEMI? Next day ECG: 2 Very instructive posts on LVH and OMI and Pseudo-OMI 1. More on LVH.
He has a history of coronary artery disease and a STEMI two years prior that was treated with primary PCI. At the time of this initial ED ECG, his symptoms were improving ECG #1 on admission to the ED The patient was not seen quickly in the ED as it was a busy shift and the ECG did not meet STEMI criteria. The below ECG was recorded.
PEARL # 3: Knowing there is an acute inferior STEMI I looked next to see if there is also acute posterior involvement ( which so often accompanies inferior MI ). But larger-than-expected Q waves in each of the inferior leads ( especially in lead III ) are probably the result of this patients ongoing acute inferior STEMI.
It is a long read, meant only for those who want to know the hidden intricacies in the concept of “Time window” in STEMI and its important Implication in patient care. [08/11, 08/11, 12:07] Dr S Venkatesan: Is the therapeutic time window for primary PCI and thrombolysis same ? [08/11, How can they be different? [08/11,
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