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A patient had a cardiacarrest with ventricular fibrillation and was successfully defibrillated. COACT: The COACT trial was fatally flawed, and because of it, many cardiologists are convinced that if there are no STEMI criteria, the patient does not need to go to the cath lab. These studies did not address OMI ECG findings!!!
Note that they finally have laid to rest the new or presumably new LBBB as a criteria for STEMI. Note that they finally have laid to rest the new or presumably new LBBB as a criteria for STEMI. Also note that they allow ST depression c/w posterior MI to be a STEMI equivalent. What is the utility of a head CT in cardiacarrest?
Shortly after arrival in the ED ( E mergency D epartment ) — she suffered a cardiacarrest. BUT — Cardiac catheterization done a little later did not reveal any significant stenosis. Figure-1: The initial ECG in today's case — obtained after successful resuscitation from cardiacarrest. ( No CP ( C hest P ain ).
This certainly looks like an anterior STEMI (proximal LAD occlusion), with STE and hyperacute T-waves (HATW) in V2-V6 and I and aVL. How do you explain the anterior STEMI(+)OMI immediately after ROSC evolving into posterior OMI 30 minutes later? This caused a type 2 anterior STEMI.
Subtle as a STEMI." (i.e., Given that this is before it is released into the circulation by reperfusion therapy, this is a massively elevated troponin. About 45 minutes after the second EKG, the patient was found in cardiacarrest. Later the next day, she went into cardiacarrest again.
Here is his ED ECG: There is obvious infero-posterior STEMI. What are you worried about in addition to his STEMI? Comments: STEMI with hypokalemia, especially with a long QT, puts the patient at very high risk of Torsades or Ventricular fibrillation (see many references, with abstracts, below). There is atrial fibrillation.
This is a troponin I level that is almost exclusively seen in STEMI. I suspect this is Type 2 MI due to prolonged severe hypotension from cardiacarrest. So this is either a case of MINOCA, or a case of Type II STEMI. If the arrest was caused by acute MI due to plaque rupture, then the diagnosis is MINOCA.
Here are three more dramatic cases that illustrate RBBB + LAFB Case 1 of cardiacarrest with unrecognized STEMI, died. Furthermore, among 35 patients with acute left main coronary artery occlusion, 9 presented with RBBB (mostly with LAH) on the admission ECG.
Circulation: Cardiovascular Interventions, Ahead of Print. BACKGROUND:Patients with ST-segment–elevation myocardial infarction but no coronary microvascular injury are at low risk of early cardiovascular complications (ECC).
This is diagnostic of infero-posterior OMI, but it is falsely negative by STEMI criteria and with falsely negative posterior leads (though they do show mild ST elevation in V4R). They were less likely to have STEMI on ECG, and more likely to be initially diagnosed as non-ACS. Circulation 2007 2. Khan et al.
The ECG shows obvious STEMI(+) OMI due to probable proximal LAD occlusion. The patient in today’s case is a previously healthy 40-something male who contacted EMS due to acute onset crushing chest pain. The pain was 10/10 in intensity radiating bilaterally to the shoulders and also to the left arm and neck. The below ECG was recorded.
Discussion See this post: STEMI with Life-Threatening Hypokalemia and Incessant Torsades de Pointes I could find very little literature on the treatment of severe life-threatening hypokalemia. If cardiacarrest from hypokalemia is imminent (i.e., When the ECG shows the effects of hypokalemia, it is particularly dangerous.
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. This ECG was recorded prehospital, and the computer read STEMI, so the medics activated the cath lab: What do you think? The ECG is consistent with high lateral STEMI. Called 911.
The patient was brought to the ED as a possible Code STEMI and was seen directly by cardiology. Similarly, STEMI guidelines call for urgent angiography for refractory ischemia or electrical/hemodynamic instability, regardless of ECG findings. On arrival, GCS was 13 and the patient complained of ongoing chest pain.
If cardiacarrest from hypokalemia is imminent (i.e., to greatly decrease risk (although in STEMI, the optimal level is about 4.0-4.5 mEq of K pushed fast and circulated theoretically would raise serum K immediately by 1.0 As I indicated above, in our cardiacarrest case, after pushing 40 mEq, the K only went up to 4.2
It is apparently fortunate that she had a cardiacarrest; otherwise, her ECG would have been ignored. Then they did an MRI: Patient underwent cardiac MRI on 10/4 that showed mildly reduced BiV systolic function. This has resulted in an under-representation of STEMI MINOCA patients in the literature. From Gue at 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. Circulation, 117, 1890–1893. [3]: So maybe she is better than I am. Smith comment: the ECG in question could be due to Brugada, even though there is a change from baseline.
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. Circulation, 117, 1890–1893. [3]: See additional image at the bottom of this post. Bicarb 20, Lactate 4.2,
AimThis study aimed to protect brain functions in patients who experienced in-hospital cardiacarrest through the application of local cerebral hypothermia. underwent emergency coronary angiography due to ST-elevation myocardial infarction (STEMI). Among the patients, 62.5%
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