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I sent this to the Queen of Hearts So the ECG is both STEMI negative and has no subtle diagnostic signs of occlusion. Non-STEMI guidelines call for “urgent/immediate invasive strategy is indicated in patients with NSTE-ACS who have refractory angina or hemodynamic or electrical instability,” regardless of ECG findings.[1]
IntroductionHypoxic liver injury (HLI) and Killip classification are poor prognostic factors in patients with ST-segment elevation myocardial infarction (STEMI). Both initial and peak AST levels increased in accordance with Killip classification along with cardiac biomarkers.
Recall from this post referencing this study that "reciprocal STD in aVL is highly sensitive for inferior OMI (far better than STEMI criteria) and excludes pericarditis, but is not specific for OMI." The ESC states that patients with suspected ACS should go to the cath lab in <2 hours "regardless of ECG or biomarker evidence of MI!!"
Step 1 to missing posterior MI is relying on the STEMI criteria. A prospective validation of STEMI criteria based on the first ED ECG found it was only 21% sensitive for Occlusion MI, and disproportionately missed inferoposterior OMI.[1] But it is still STEMI negative. A 15 lead ECG was done (below). In a study last year, 14.4%
His ECG was repeated at this point: This shows a well developed anterior STEMI. To not see these findings is very common, and this patient would be given the diagnosis of NonSTEMI, with subsequent development of STEMI. It is not a missed STEMI, but it is a missed coronary occlusion. The peak troponin I was over 100.
The "criteria" for posterior STEMI are 0.5 Is it STEMI or NonSTEMI? It was opened and stented with a door to balloon time of about 120 minutes (this is long for STEMI, but very short for a high risk Non STEMI). This is from the 2014 ACC/AHA guidelines. The troponin I returned at 4.1 mm STE in one lead.
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