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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. Similarly, if a patient with known CAD presents with refractory ischemic chest pain, the ECG barely matters: the pre-test likelihood of acute coronary occlusion is so high that they need an emergent angiogram.
The patient presented to an outside hospital An 80yo female per triage “patient presents with chest pain, also hurts to breathe” PMH: CAD, s/p stent placement, CHF, atrial fibrillation, pacemaker (placed 1 month earlier), LBBB. Most large STEMI have peak troponin I in the 20.0 There are hyperacute T-waves in V5 and V6. Next trop in AM.
Furthermore, there was no family history of early CAD, MI, or sudden cardiac death. BP 142/100 HR 90 RR 16 (BBS CTA) SpO2 99 (RA) Dstick 110 My colleagues noted the ST-depression in the respective leads, as well, and STEMI activated to the nearest PCI center. 1] Here is the admitting ED ECG after cancellation of Code STEMI.
Moreover, he had no pertinent medical history to report in terms of CAD, HTN, HLD, or DM, for example. A prehospital STEMI activation was transmitted to the closest PCI center, and 324mg ASA was administered. His vital signs were unremarkable, and the lung fields were free of fluid congestion during auscultation. 2] Driver, B.
Case history A middle-aged woman with a history of HTN, but no prior CAD, presented to the ED with chest pain. The criteria of Armstrong et al. would require the ST/S ratio to be 25% for diagnosis of STEMI in LVH. Can you diagnose an ACO (STEMI) when you also have LVH? One retrospective analysis by Armstrong et al.
A middle aged male with no h/o CAD presented with one week of crescendo exertional angina, and had chest pain at the time of the first ECG: Here is the patient's previous ECG: Here is the patient's presenting ED ECG: There is isolated ST depression in precordial leads, deeper in V2 - V4 than in V5 or V6. There is no ST elevation.
So I went to look at the chart and here is the history: This patient with no h/o CAD had a couple of episodes of chest pain during the day, then presented with one hour of substernal chest pain that had some reproducibility but also improved from 10/10 to 5/10 with nitroglycerine. Fesmire et al. Wang T, Zhang M, Fu Y, et al.
He had significant history of CAD with CABG x5, and repeat CABG x 2 as well as a subsequent PCI of the graft to the RCA (twice) and of the graft to the Diagonal. Here is his ED ECG: There is obvious infero-posterior STEMI. What are you worried about in addition to his STEMI? Most recent echo showed EF of 60%. Learning Points: 1.
However, a smooth tapering of the mid-RCA was seen, highlighted in red below: How do we explain the MI if no sign of CAD was found? This MI wasn’t caused by a ruptured plaque of CAD - it was a coronary artery dissection of the RCA. A recent study found that SCAD causes almost 20% of STEMI in young women. A study by Hassan et al.
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. The patient proceeded to cath where all coronaries were described as normal with no evidence of any CAD, spasm, or any other abnormality. So maybe she is better than I am.
STEMI , ST-segment elevation acute myocardial infarction ). 1 Initial diagnosis of STEMI ECG Management Recommendation Level of evidence A 12-lead ECG should be interpreted immediately (within 10 minutes) at first medical contact. I C If possible, patients should bypass non-PCI centres to a PCI-capable centre.
This is technically a STEMI, with 1.5 However, I think many practitioners might not see this as a clear STEMI, and would instead call this "borderline." They collected several repeat ECGs at the outside hospital before transport: None of these three ECGs meet STEMI criteria. This ECG was recorded on arrival: What do you think?
This is diagnostic of inferior MI, though does not meet millimeter criteria for "STEMI." He had a family history of early CAD and occasional drug and tobacco use. He was worried for inferior MI and ordered another, which was recorded 15 minutes later: Now clearly and obviously diagnostic of inferior STEMI.
When total LM occlusion does present with STE in aVR, there is ALWAYS ST Elevation elsewhere which makes STEMI obvious; in other words, STE is never limited to only aVR but instead it is part of a massive and usually obvious STEMI. All are, however, clearly massive STEMI. This is her ECG: An obvious STEMI, but which artery?
Reference on Troponins: Xenogiannis I, Vemmou E, Nikolakopoulos I, et al. J Electrocardiol [Internet] 2022;Available from: [link] Cardiology opinion: Takotsubo Cardiomyopathy (EF 30-35%) V Fib Cardiac arrest Prolonged QTC NSTEMI (Smith comment: is it NSTEMI or is it Takotsubo? -- these are entirely different) Moderate single-vessel CAD.
A middle-aged male with h/o CAD and stents presented with typical chest pressure. 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. So there is pathologic ST elevation here, consistent with anterolateral STEMI. Called 911.
A man in his 70s with past medical history of hypertension, dyslipidemia, CAD s/p left circumflex stent 2 years prior presented to the ED with worsening intermittent exertional chest pain relieved by rest. Hayakawa A, Tsukahara K, Miyagawa S, et al. Written by Nathanael Franks MD, reviewed by Meyers, Smith, Grauer, etc. Am J Emerg Med.
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. In the largest study looking at this topic by Mizusawa et al., There was a 0.9%
No family history of sudden cardiac death, cardiomyopathy, premature CAD, or other cardiac issues. 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. Pericarditis?
These findings are very subtle but suspicious for LAD occlusion, as we have seen in many similar (but less difficult) cases on this blog: A man in his sixties with chest pain at midnight with undetectable troponin How long would you like to wait for your Occlusion MI to show a STEMI? He also had non-acute CAD of the RCA (50%) and LCX (50%).
Clinical Course The paramedic activated a “Code STEMI” alert and transported the patient nearly 50 miles to the closest tertiary medical center. 2 The astute paramedic recognized this possibility and announced a CODE STEMI. Taglieri N, Marzocchi A, Saia F, et al. Kosuge M, Ebina T, Hibi K, et al. What do you see?
This study from Herzog et al (from our own Hennepin County Medical Center) included patients from a national registry and compared 3049 patients on dialysis admitted and eventually found to have acute MI compared with 534,395 patients not on dialysis admitted with an eventual diagnosis of acute MI. Herzog et al.
Scattered other nonobstructive CAD. This patient does not show up in the STEMI registry, and the time to reperfusion will likely not be identified as the problem that it was. de Winter et al in N Engl J Med 359:2071-2073, 2008. YOU TOO CAN HAVE THE PM Cardio AI BOT!!
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