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Here is his ED ECG: There is obvious infero-posterior STEMI. What are you worried about in addition to his STEMI? There is also bradycardia. Bradycardia puts patients at risk for "pause-dependent" Torsades de Pointes. Bradycardia puts patients at risk for "pause-dependent" Torsades de Pointes. Learning Points: 1.
I did not think that the T-waves in V2 and V3 are hyperacute and I still do not--I disagree with Ken below--I think they are normal , especially in the context of bradycardia. Their apparently excessive length (QT interval) is due to bradycardia. They do not have much bulk. A corrected QT would be normal.
He reports that this chest pain feels different than prior chest pain when he had his STEMI/OMI, but is unable to further describe chest pain. I sent it to 5 of my OMI friends without any clinical information or outcome and all 5 independently responded with exactly the same diagnosis: "reperfused inferior OMI". No chamber enlargement.
The receiving emergency physician consulted with interventional cardiology who stated there was no STEMI. Opioids associate with worse outcomes in myocardial infarction , probably because they eliminate the pain signal that informs the clinician of the urgency of revascularization. Is there STEMI? Do not treat AIVR. Moffat, M.
Repeat ECG showing no STEMI, only non-specific ST-segment and T-wave abnormalities, unchanged from prior" Transferred to surgery for exploration but diagnostic studies were too indeterminate to be certain of intra-abdominal pathology. Trop T now very high, well into the range one sees with a STEMI; very unusual in type II MI.
Here is his ED ECG: There is bradycardia with a junctional escape. There is an obvious inferior posterior STEMI(+) OMI. Case continued A bedside ultrasound showed diminished LV EF and of course bradycardia. Results Of 149 patients with inferior STEMI , 43 (29%) had RVMI and 106 (71%) did not. What is the atrial activity?
Sinus bradycardia, normal conduction, normal axis, normal R wave progression, no hypertrophy. 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]
The provider contacted cardiology to discuss the case, but cardiology "didn't think it was a STEMI, didn't think he needed emergent cath." Could this outcome have been prevented with emergent cath? JAMA 2000) showed that 1/3 of patients with STEMI, and 1/3 of patients with NSTEMI, present without chest pain. Canto et al.
These kinds of cases were excluded from the study as obvious anterior STEMI. --QTc Case 1 Acute anterior STEMI from LAD occlusion, or Benign Early Repolarization (BER)? Appropriately, the physicians repeated the ECG 20 minutes later and it was diagnostic of anterior STEMI. Why bradycardia? QTc is the computer measurement.
It doesn’t meet any conventional STEMI criteria, but there is patently obvious increased area under the curve. Could there have been a different outcome if the crews immediately recognized OMI – versus a shortened PR-interval – and commenced with pre-hospital Cath Lab activation? Is this OMI?
Here is PM Cardio's Queen of Hearts interpretation (AI ECG interpretation trained by Meyers, Smith, and PM Cardio team using thousands of cases and their outcomes): The output number ranges from 0 to 1, with numbers closer to zero meaning likely NOT OMI, and numbers closer to 1 meaning OMI.
Triage physician interpretation: -sinus bradycardia -lateral ST depressions While there are lateral ST depressions (V5, V6) the deepest ST depressions are in V4. Recall that air is a poor conductor of electricity and will, therefore, generate smaller amplitudes on posterior leads (hence why STEMI criteria requires only >0.5
There’s sinus bradycardia, first degree AV block, normal axis, delayed R wave progression, and normal voltages. There’s minimal concave ST elevation in III which does not meet STEMI criteria, so this ECG is "STEMI negative". Use STEMI criteria to identify acute coronary occlusion: the ECG was STEMI negative 2.
Theres sinus bradycardia, borderline PR interval, narrow QRS; normal axis/R wave progression; low precordial voltages, and subtle peaked T waves (most obvious in V2, but all T waves are symmetric with a narrow base). Theres no prior ECG to compare - but the bradycardia, prolonged PR and peaked T waves could all be from hyperkalemia.
Despite the baseline artifact theres sinus bradycardia, convex ST elevation in III, reciprocal ST depression in aVL and possible anterior ST depression indicating inferoposterior OMI. STEMI criteria are only 43% sensitive for OMI. Beware confusing the diagnosis of posterior STEMI by using posterior leads.
Within ten minutes, she developed bradycardia, hypotension, and ST changes on monitor. Bradycardia and heart block are very common in RCA OMI. Was her outcome to be expected for ostial RCA OMI? There was indication of parasympathetic overdrive ( the acute inferior STEMI with profound bradycardia and junctional escape ).
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