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The ECG did not meet STEMI criteria, and the final cardiology interpretation was “ST and T wave abnormality, consider anterior ischemia”. There’s only minimal ST elevation in III, which does not meet STEMI criteria of 1mm in two contiguous leads. But STEMI criteria is only 43% sensitive for OMI.[1]
Written by Bobby Nicholson What do you think of this “STEMI”? or basilar ischemia. Second, although there is a lot of ST Elevation which meets STEMI criteria, especially in V3-4, the ST segment is extremely upwardly concave with very large J-waves (J-point notching). 2016 Nov;34(11):2182-2185. Epub 2016 Aug 27.
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?
When “spot diagnosing” precordial ST-depression I instinctively evaluate aVR for any corresponding ST-elevation to see if an emerging pattern of broad subendocardial ischemia can be appreciated, in which the ST-depression should be otherwise global and demonstrably maximal in Leads II and V5. However, in this context (i.e. is present.
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).
A prior ECG from 1 month ago was available: The presentation ECG was interpreted as STEMI and the patient was transferred emergently to the nearest PCI center. BOTTOM Line: It can at times be extremely challenging to distinguish between anterior ST elevation from a benign Brugada Phenocopy pattern vs an acute anteroseptal STEMI.
This strongly suggests reperfusing RCA ischemia. Troponins, echocardiogram An echocardiogram showed inferobasilar hypokinesis, further supporting a diagnosis of regional ischemia , likely of the area supplied by the RCA. Angie Lobo ( @aloboMD ) (For open-access reviews of this literature, see Saw 2016 , Saw 2017 , or Hayes 2018.)
2) The STE in V1 and V2 has an R'-wave and downsloping ST segments, very atypical for STEMI. Cardiology was consulted and they agreed that the EKG had an atypical morphology for STEMI and did not activate the cath lab. Smith comment: 1) Brugada ECG may have ST shifts in limb leads as well as precordial leads. Bicarb 20, Lactate 4.2,
Figure 1-1 My colleague, a faithful student of ECG interpretation, handed me the tracing and said that it warranted STEMI activation because of apparent terminal QRS distortion (TQRSD) in V2. ASA 324mg was administered while a STEMI activation was simultaneously transmitted to the nearest PCI center. Attached is the first ECG.
She had this ECG recorded: Obvious massive anterior STEMI She was quickly brought to the critical care area and the cath lab was activated. Here is the ECG at 25 minutes: Terrible LAD STEMI (+) OMI So a CT scan was done which of course showed a normal aorta. This time the Queen of Hearts interpreted: No STEMI or Equivalent.
He is a STEMI patient (1 year old) with mild LV dysfunction and thinning of IVS and anterior wall. Suddenly, as I finish writing this, a big fact struck me hard , i.e., even a well-done PCI in sophisticated core labs with meticulous care struggled to beat OMT in a barrage of landmark trials (like COURAGE, ISCHEMIA, ORBITA).
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