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A patient had a cardiacarrest with ventricular fibrillation and was successfully defibrillated. This is FAR LESS than all other studies of shockable arrest. Coronary Angiography after CardiacArrest without ST-Segment Elevation. The proof of this is that only 5% of patients enrolled had acute coronary occlusion.
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. (
ST depression is common BOTH after resuscitation from cardiacarrest and during atrial fib with RVR. Again, it is common to have an ECG that shows apparent subendocardial ischemia after resuscitation from cardiacarrest, after defibrillation, and after cardioversion. The patient was cardioverted. This was done.
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. TIMI-0 flow.
The last section is a detailed discussion of the research on aVR in both STEMI and NonSTEMI. The additional ST Elevation in V1 is not usually seen with diffuse subendocardial ischemia, and suggests that something else, like STEMI from LAD occlusion, could be present. Here is an article I wrote: Updates on the ECG in ACS. see below).
An echocardiogram confirmed aortic stenosis with a large pressure gradient. Thus, this patient had increased ST elevation (current of injury) superimposed on the ST elevation of LVH and simulating STEMI. The next day, and angiogram showed normal coronary arteries. He awoke and did well.
RBBB in acute STEMI has a very high mortality. Angiography revealed a very tight LAD stenosis with some flow (confirming the reperfusion that we see on the ECG). Were it not for this prehospital ECG and the cardiacarrest, the diagnosis may have been significantly delayed.
The ECG shows obvious STEMI(+) OMI due to probable proximal LAD occlusion. Angiography : LMCA — 90-99% osteal stenosis. LCx — 50-69% stenosis of the 1st marginal branch; with 100% distal LCx occlusion. The patient in today’s case is a previously healthy 40-something male who contacted EMS due to acute onset crushing chest pain.
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? His response: “subendocardial ischemia.
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.
There is a very small amount of STE in some of the anterior, lateral, and inferior leads which do NOT meet STEMI criteria. The case was reviewed by all parties, and it was stated correctly that the ECG does not meet the STEMI criteria. The STEMI vs. NSTEMI paradigm is not the best way to decide who needs emergent reperfusion therapy.
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. She was defibrillated and resuscitated. Smith: this ECG and clinical presentation is diagnostic of LAD Occlusion.
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.
He had a previous MI with cardiacarrest 2 years prior. Important Learning Point: "STEMI" is defined by millimeter criteria (1 mm in limb leads), which this does not meet. Therefore it is not a STEMI. The ST depression may be the most visibly obvious sign of STEMI. Some are STEMI-equivalents. RCA: dominant.
But limitation of this ST elevation to a single lead is not consistent with any distribution of a STEMI. Unfortunately — the patient abruptly developed hypoxemia, followed by cardiacarrest with PEA. It was thought that this action precipitated the patient's desaturation, and led to his cardiacarrest.
Could this be Septal STEMI (STE in V1 and aVR, with reciprocal ST depression in V4-V6?), In Septal STEMI , transmural ischemia of the septum is recorded by the overlying lead V1 as ST Elevation. Lead III is also on the right and might manifest ST Elevation in Septal STEMI. with ADDED STE in III?
A prehospital ECG was recorded (not shown and not seen by me) which was worrisome for STEMI. A previous ECG from 4 years prior was normal: This looks like an anterior STEMI, but it is complicated by tachycardia (which can greatly elevate ST segments) and by the presentation which is of fever and sepsis.
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