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Here is his ED ECG at triage: Obvious high lateral OMI that does not quite meet STEMI criteria. This confirms that the pain was ischemia and is now resovled. He does have a recently diagnosed PE, and has not been taking his anticoagulation due to cost. He was given aspirin and sublingual nitro and the pain resolved.
This EKG is diagnostic of transmural ischemia of the inferior wall. If it is angina, lowering the BP with IV Nitroglycerine may completely alleviate the pain and the (unseen) ECG ischemia. Transmural ischemia (as seen with the OMI findings on ECG) is not very common with demand ischemia, but is possible.
I sent this to the Queen of Hearts So the ECG is both STEMI negative and has no subtle diagnostic signs of occlusion. Non-STEMI guidelines call for “urgent/immediate invasive strategy is indicated in patients with NSTE-ACS who have refractory angina or hemodynamic or electrical instability,” regardless of ECG findings.[1]
See my formula for differentiating anterior LV aneurysm (that is to say, persistent ST elevation after old MI) from acute anterior STEMI. Both support acute anterior STEMI. This is clearly an oversimplification, as many patients have pain for very long periods that is not irreversible infarction but rather ongoing angina.
This is a 45 yo male who had an inferior STEMI 6 months prior, was found to have severe LAD and left main disease, and was supposed to be set up for CABG a few weeks later, but did not follow up. But it could be anterior STEMI. 40% of anterior STEMI has upward concavity in all of leads V2-V6. is likely anterior STEMI).
This is all but diagnostic of STEMI, probably due to wraparound LAD The cath lab was activated. This was clearly severe subepicardial ischemia causing ST Elevation, but it was not of a long enough duration to result in measurable infarct. Therefore this is " Transient ST Elevation Unstable Angina." Why is this important?
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.
The ECG in the chart was read as "no obvious ST changes," (even though no previous ECG was available) and the formal read by the emergency physicians was: "ST deviation and moderated T-wave abnormality, consider lateral ischemia." New ST elevation diagnostic of STEMI [equation value = 25.3 Computerized QTc = 417. Gottlieb SO, et al.
This appears to be a classic Wellens' ECG, Pattern A, with terminal T-wave inversion in V2-V4, preserved R-waves, and it appears to be Wellens' syndrome, as it occurred after resolution of typical angina pain. Wellens' syndrome represents the aftermath of an unrecorded occlusion (STEMI) with spontaneous reperfusion.
Here is the prehospital ECG, with pain: Hyperacute anterolateral STEMI The medics had activated the cath lab and the patient went for angiogram and had a 95% stenotic LAD with TIMI-3 flow. For those who depend on echocardiogram to confirm the ECG findings of ischemia, this should be sobering. Type B waves are deeper and symmetric.
It has been estimated that in the aggregate, they occur at a rate of about 3 per 1000 patients with acute MI, and most of these events occur in patients with STEMI. A mong patients with STEMI, ventricular septal rupture is the most common and free wall rupture is the least common.
The patient was given aspirin, heparin, morphine, and ondansetron and and transferred to a PCI-capable facility for a diagnosis of "unstable angina" with dynamic ECG changes. The receiving emergency physician consulted with interventional cardiology who stated there was no STEMI. Is there STEMI? What is the rhythm? Moffat, M.
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?
Some persistently denied that the T-wave in V2 was a specific sign of ischemia. But beware the few false negatives, especially when there are hyperacute T-waves but no ST elevation (see Case 2 below): Formula to differentiate Normal Variant ST Elevation (Early Repolarization) from Anterior STEMI. A positive troponin is useful.
The baseline ECG is basically normal with no ischemia. You can see in the lead-specific analysis that she "sees" the STD in V5, V5, and II, with STE in aVR as signs of "Not OMI", because subendocardial ischemia pattern is not the same as OMI. In my opinion, I think it looks more like subendocardial ischemia. As per Drs.
Post by Smith and Meyers Sam Ghali ( [link] ) just asked me (Smith): "Steve, do left main coronary artery *occlusions* (actual ones with transmural ischemia) have ST Depression or ST Elevation in aVR?" All are, however, clearly massive STEMI. This is her ECG: An obvious STEMI, but which artery?
The HEART and EDACS scores are helpful to risk stratify patients with chest pain, but they hinge on accurate ECG interpretation: a low score doesn’t apply if the ECG shows STEMI(+)OMI, and shouldn’t be used for STEMI(-)OMI or OMI reperfusion either 2. Was this objective evidence of inducible ischemia accompanied by chest pain?
A middle-aged woman had intermittent angina for 48 hours, then onset of constant, crushing chest pain for 1.5 cm diameter in the apex The presence of thrombus led the clinicians to state that this was a "late presentation STEMI." hours when she called 911. LV Thrombus , 1.5 0 0 1 95 544 MMRF 4 1 638 14.0
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.’
Additional Teaching Points: Type-2 MI ( M yocardial I nfarction ) — is defined by an increase in troponin with evidence of ischemia that is not due acute coronary disease, but which instead results from a mismatch in oxygen supply and demand ( Smilowitz et al — Coron Artery Dis 29(1):46-52, 2018 ).
It is equivalent to a transient STEMI. Now you have ECG and troponin evidence of ischemia, AND ventricular dysrhythmia, which means this is NOT a stable ACS. It they are static, then they are not due to ischemia. This is better evidence for ischemia than any other data point. Again, cath lab was not activated.
Takotsubo is a sudden event, not one with crescendo angina. 9 This dissociation between the degree of stenosis and the propensity to provoke an acute coronary syndrome helps to explain why myocardial infarction often occurs without being heralded by the demand-induced symptoms of angina that would result from a high-grade stenosis.
They recorded a prehospital ECG and diagnosed STEMI and activated the cath lab prehospital. The patient did not report angina with stress. This ST-T wave appearance in the lateral chest leads of ECG #2 is consistent with L V “ S train” vs ischemia. I heard that a prehospital cath lab activation was on its way.
A middle aged patient who was 3 weeks s/p STEMI came from cardiac rehab where he developed some chest pain, dyspnea and weakness on the treadmill. There is no acute STEMI. This is diagnostic of recent, reperfused STEMI. This is diagnostic of recent, reperfused STEMI. Acute STEMI would have upright T-waves.
Relationship between Ischemia and arrhythmia While the relationship between Ischemia and VT is really complex, the term “Ischemic VT” itself adds more twists. Even here, it is the associated factors, like hypoxia or acidosis are the triggers which of course are resultant of Ischemia.
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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