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The Queen of Hearts disagrees, diagnosing OMI with high confidence: Case Continued: The EKG was not immediately recognized by the emergency provider, who ordered a CT scan to rule out aortic dissection at 1419. Most STEMI have peak troponin I over 1000 ng/L and most NSTEMI below that level.
Smith comment: This patient did not have a bedside ultrasound. Had one been done, it would have shown a feature that is apparent on this ultrasound (however, this patient's LV function would not be as good as in this clip): This is recorded with the LV on the right. Look at the aortic outflow tract. What do you see?
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. aVR ST segment elevation: acute STEMI or not? J Electrocardiol 2013;46:240-8 2. Left main?
The next morning the patient went for his routine echocardiogram, where the operator noticed a dilated aortic root at 5.47 cm with severe aortic insufficiency. The team was notified and they ordered a stat aortagram which showed type A aortic dissection from the aortic valve to the iliacs. Pericarditis?
Due to the severity of the pain and the high BP, they obtained an aortic dissection CT. Here is the repeat ECG at 52 minutes after arrival to triage: Obvious posterolateral STEMI Angiographic findings: 1. Regional wall motion abnormality-inferolateral (this is the formal ultrasound location of a posterior wall motion abnormality).
Thus, this is BOTH an anterior and inferior STEMI in the setting of RBBB. How old is this antero-inferior STEMI? Although acute anterior STEMI frequently has narrow QR-waves within one hour of onset (1. the presence of such well developed, wide, anterior Q-wave suggests completed transmural STEMI. Could it be acute (vs.
It may be difficult to read STEMI in the setting of RBBB. There is, however, a long QT also, with abnormal T-waves, but this is not STEMI. An elderly patient with a ruptured abdominal aortic aneurysm: Formal ECG Interpretation (final read in the chart!) : "Inferior ST elevation, lead III, with reciprocal ST depression in aVL."
50% of LAD STEMIs do not have reciprocal findings in inferior leads, and many LAD OMIs instead have STE and/or HATWs in inferior leads instead. The ECG easily meets STEMI criteria in all leads V2-V6, as well. CT angiogram chest: no aortic dissection or pulmonary embolism. 24 yo woman with chest pain: Is this STEMI?
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. And almost all of them could be detected by bedside ultrasound.
I suspect pulmonary edema, but we are not given information on presence of B-lines on bedside ultrasound, or CXR findings. Supply-demand mismatch can cause ST Elevation (Type 2 STEMI). Also see these posts of Type II STEMI. Truly, the Marquette 12 SL algorithm correctly identifies this STEMI. Management?
Case continued A bedside cardiac ultrasound revealed grossly preserved left ventricular function, no appreciable wall motion abnormality, pericardial effusion, or obvious valvular abnormality. The terminal part of the T-wave is inverted in lead III, and reciprocally terminally upright in lead aVL. Another EKG was also obtained.
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