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4,5] We have now formally studied this question: Emergency department Code STEMI patients with initial electrocardiogram labeled ‘normal’ by computer interpretation: a 7-year retrospective review.[6] have published a number of warnings about the previous reassuring studies.[4,5]
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). 2017 Sep-Oct;50(5):561-569. Epub 2017 Apr 19.
The ECG shows obvious STEMI(+) OMI due to probable proximal LAD occlusion. There is no definite evidence of acute ischemia. (ie, Simply stated — t he patient was having recurrent PMVT without Q Tc prolongation, and without evidence of ongoing transmural ischemia. ( The below ECG was recorded.
Learning Point: Concordant ST segment elevation can arise from profound ischemia triggered by ventricular tachycardia (VT), or it may represent an exaggerated basal ST change accompanying tachycardia. The patient rapidly regained consciousness, reporting no residual pain. A peak troponin level of 70 ng/L was observed.
There is normal R-wave progression in the precordial leads with no evidence of ischemia. Troponin T peaked at 2074 ng/L (very high, typical of OMI/STEMI). 21, 2017 ). Here the image quality is enhanced using the PM Cardio app. What do you think? The presenting ECG shows SR with narrow QRS complexes.
There is broad subendocardial ischemia as demonstrated by STE aVR with concomitant STD that almost appears appropriately maximal in Leads II and V5. There is LBBB-like morphology with persistent patterns of subendocardial ischemia. This worried the crew of potential acute coronary syndrome and STEMI was activated pre-hospital.
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. 2017 AHA/ACC/HRS guideline for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death. So maybe she is better than I am.
While this ECG is negative for “posterior STEMI”, the resolution of anterior ST depression (accompanied by the troponin elevation) confirms posterior OMI with spontaneous reperfusion. The second opportunity to make the diagnosis and expedite angiography was missed because the ECG never met STEMI criteria and continued to be labeled ‘normal.’
European Heart Journal 38(41):3082-3089; November 1, 2017. And, in cases like the elderly patient with new-onset chest pain presented here — definitive diagnosis of acute STEMI is sometimes deceptively easy. BOTTOM LINE: Despite cardiac pacing — ECG #2 is diagnostic of a very large acute anterior STEMI.
A prehospital STEMI activation was transmitted to the closest PCI center, and 324mg ASA was administered. The attending crews were concerned for an ACS-equivalent of LAD occlusion and initiated a prehospital STEMI activation to the closest PCI center. It’s important to stress the presence of a normal QRS (i.e., 2] Driver, B.
These kinds of cases were excluded from the study as obvious anterior STEMI. --QTc J Electrocardiology 50(5):561-569; September/October 2017. Case 1 Acute anterior STEMI from LAD occlusion, or Benign Early Repolarization (BER)? Case 4 Transient STEMI, serial ECGs prehospital to hospital, all troponins negative (less than 0.04
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,
PCI mid LCx So this is an OMI (Occlusion Myocardial Infarction), but not a STEMI Echo: Decreased left ventricular systolic performance, mild/moderate. This figure comes from the Diamond T study (all type 1 MI were NSTEMI, not STEMI): Notice that the 6 hour value (far right) is very low for type 2 MI. Angiogram: LM 30% ostial.
JACC 69(23):1694-1703; April 4, 2017. But lead V2 has a worrisome amount of ST elevation, and in a chest pain patient, I would be worried about STEMI. S-wave is in V2 = 17 mm S-wave V4 = 9 mm Total = 26 (not greater than 28), so not LVH by the new rule! Nevertheless, it has the look of LVH. Peguero JG et al.
This doesn’t meet STEMI criteria so in the current paradigm there’s no urgency to getting an angiogram. Even though they were passed the 12 hour mark traditionally associated with reperfusion benefits, ongoing ischemia requires emergent angiogram On assessment, the patient appeared uncomfortable, leaning forward in his chair.
ECG met STEMI criteria and was labeled STEMI by computer interpretation. J waves can also be induced by Occlusion MI (5), STEMI mimics including takotsubo and myocarditis complicated by ventricular arrhythmias (6, 7), and subarachnoid hemorrhage with VF (8). Take home : Not all STEs are STEMIs or OMIs. What do you think?
A 12-lead was recorded, showing "STEMI," but is unavailable. Moreover, if you know that catastrophic intracranial hemorrhage can result in an ECG that mimics STEMI, then you know that this patient probably has a severe intracranial hemorrhage. She was BVM ventilated and suctioned. Shortly thereafter, pulses were lost.
50% of LAD STEMI have Q-waves by one hour. Smith : In limb leads, the ST vector is towards lead II (STE lead II STE lead III, which is more likely with pericarditis than with STEMI). There were no other causes of dyspnea apparent and thus we can assume that myocardial ischemia started 6 days prior. See Raitt et al.:
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