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For full discussion of this case — See ECG Blog #351 — == The ECG in Figure-1 — was obtained from a previously healthy older man who contacted EMS ( E mergency M edical S ervices ) because of "chest tightness" that began ~1 hour earlier. ECG Blog #205 = The Systematic Approach I favor. . =
For full discussion of this case — See ECG Blog #392 — == The ECG in Figure-1 was obtained from a man in his 60s — who described the sudden onset of "chest tightness" that began 20 minutes earlier, but who now ( at the time this ECG was recorded ) — was no longer having symptoms. ECG Blog #387 — Dynamic change in 2 minutes.
For full discussion of this case — See ECG Blog #292 — == The 2 ECGs shown in Figure-1 were obtained from a man in his 30s — who presented to the ED ( E mergency D epartment ) with chest pain that began several hours earlier. Related ECG Blog Posts to Today’s Case: ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
By the P s, Q s, 3 R Approach ( which I review in ECG Blog #185 ): Lots of P waves are present — being well seen in the long lead II rhythm strip. This slight variation in sinus P wave regularity tends to be greater when a 2nd- or 3rd-degree AV block is present ( called ventriculophasic sinus arrhythmia — as shown in ECG Blog #344 ).
These tall T waves are associated with flattening ( straightening ) of the ST segment in the inferior leads — with slight S T elevation in leads V2-thru-V6 ( albeit not enough to qualify as a "STEMI" — Akbar et al, StatPearls, 2023 ). This point is discussed in detail in the March 24, 2023 post of Dr. Smith’s ECG Blog ).
Voltage for LVH is satisfied — at least by Peguero Criteria ( Sum of deepest S in any chest lead + S in V4 ≥23 mm in a woman — as discussed in ECG Blog #73 ). Smith's ECG Blog — Drs. Figure-3: Selected sets of V1,V2 leads from the examples of Precordial Swirl provided in the October 15, 2022 post in Dr. Smith's ECG Blog.
PEARL # 3: While not 100% predictive — seeing a significant negative component to the P wave in these leads ( as per the YELLOW arrows in Figure-2 ) — suggests that the V1,V2 electrodes may be placed 1 or 2 interspaces too high on the chest ( See ECG Blog #274 — for more on too high placement of the V1,V2 electrode leads ).
PEARL # 1: Although seeing an elevated Troponin would provide additional support for immediate cardiac catheterization — the clinical reality is that the initial Troponin reading will not always be elevated in patients with acute coronary occlusion ( See March 24, 2023 post in Dr. Smith's ECG Blog ).
Does the ECG represent STEMI-negative OMI findings? ischemia) or it can be secondary to abnormal depolarization (e.g Discussion: The ECG in today's case does not have typical ST depression vector of diffuse subendocardial ischemia. ST depression has a variety of different causes other than ischemia.
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. For more on MINOCA — See My Comment in the November 16, 2023 post in Dr. Smith's ECG Blog ). He was given aspirin and sublingual nitro and the pain resolved.
This ST depression appears to be maximal in leads V3-to-V5 — which could reflect acute posterior OMI ( O cclusion-based M yocardial I nfarction ) — most probably with multi -vessel disease ( ie, diffuse subendocardial ischemia suggested by the ST depression with ST elevation in aVR>V1 ). ECG Blog #316 — The patient died.
In this ECG Cases blog we look at 10 patients with shortness of breath, and discuss how the ECG can be used to help diagnose cardiac, respiratory and metabolic emergencies.
R elated E CG B log P osts to Today’s Case : ECG Blog #205 — Reviews my S ystematic A pproach to 12-lead ECG Interpretation. ECG Blog #193 — illustrates use of the M irror T est to facilitate recognition of acute Posterior MI. ECG Blog #294 — How to tell IF the "culprit" artery has reperfused.
Although this " Imbalance " of precordial T waves is not see n very often — in the “right” clinical setting, it has been associated with recent OMI ( O cclusion-based MI ) , most often from a LCx culprit artery ( See Manno et al: JACC 1:1213, 1983 — and the July 17, 2013 post by Salim Rezaie in ALiEM — and ECG Blog #350 ).
Interpretation : diagnostic of acute anterior OMI with STE less than STEMI criteria in V1-V4, hyperacute T waves in V2-V4, and suspiciously flat isoelectric ST segments in III and aVF suspicious for reciprocal findings. Now it even meets STEMI criteria, and HATWs continue to inflate. So the cath lab was not activated. Ongoing OMI.
== P lease N OTE : After today — No new ECG Blog posts for 2- to -3 weeks. — I will also not be prompt in replying to emails. == All material on this ECG Blog site remains open! IF you scroll down a little on the right-hand column of this blog — You'll see a lot of icons. Figure-1: The initial ECG in today's case.
To EMPHASIZE: Despite there not being "enough" ST elevation to satisfy millimeter-based criteria for an acute "STEMI" in ECG #1 — this initial ECG is absolutely diagnostic of OMI. ECG Blog #193 — illustrates use of the M irror T est to facilitate recognition of acute Posterior MI. ECG Blog #190 — Reviews the concept of RV MI.
The overall ST-T wave appearance in this lead looks more like LV “strain” than ischemia. In a patient with new chest pain — this ST-T wave appearance in lead V2 of ECG #2 is consistent with a positive " Mirror " Test ( as described in ECG Blog #285 — as well as in other Related ECG Blog links provided below ).
Cath lab declined as it is not a STEMI." There is probably a trickle of flow which is why there is both subendocardial ischemia (ST depression) and early subepicardial ischemia (hyperacute T-waves). And now this finding is even formally endorsed as a "STEMI equivalent" in the 2022 ACC guidelines!!! It is a mass delusion.
By the P s, Q s, 3 R Approach ( as reviewed in ECG Blog #185 ): The Q RS complex is obviously wide. ie, Severe subendocardial ischemia from sustained VT in a patient severe apical cardiomyopathy resulted in a peak troponin >31,000 ng/L in today's case ). . = I do not see P waves. The rhythm is R egular — at a R ate of ~230/minute.
Looking at the location of ST elevation ( ie, in the inferior leads — and in V4,5,6 ) — and the location of ST depression ( ie, in leads I,aVL; V1,V2 ) — this ECG picture suggests an ongoing acute infero - postero - lateral STEMI. ECG Blog #265 — Reviews a case of Shark-Fin ST Elevation. What is S hark F in M orphology ?
The ECG did not meet STEMI criteria, and the final cardiology interpretation was “ST and T wave abnormality, consider anterior ischemia”. There’s only minimal ST elevation in III, which does not meet STEMI criteria of 1mm in two contiguous leads. But STEMI criteria is only 43% sensitive for OMI.[1]
This was sent by an undergraduate (not yet in medical school, but applying now) who works as an ED technician (records all EKGs, helps with procedures, takes vital signs) and who reads this blog regularly. This EKG is diagnostic of transmural ischemia of the inferior wall. Edited by Smith He also sent me this great case. Smith SW.
The ECG shows severe ischemia, possibly posterior OMI. But cardiac arrest is a period of near zero flow in the coronary arteries and causes SEVERE ischemia. It takes time for that ischemia to resolve. Cardiac arrest #3: ST depression, Is it STEMI? And what do you want to do?
Looking Systematically ( as per ECG Blog #205 ): The rhythm is sinus. I thought this finding consistent with the finding of ST depression in lateral leads I; V4,V5,V6 — and possibly indicative of multivessel disease ( ie, Diffuse Subendocardial Ischemia — as discussed in ECG Blog #400 ).
The admission and discharge diagnosis both attributed the ECG changes and echo findings to ischemia. The biggest problem with STEMI criteria are false negatives – because this costs patient’s myocardium, with greater mortality and morbidity. baseline ECGs may fluctuate over time, and not necessarily represent dynamic ischemia 4.
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]
The interventional cardiologist then canceled the activation and returned the patient to the ED without doing an angiogram ("Not a STEMI"). I advised that perhaps posterior leads would help to persuade the interventionalist, since the 2022 ACC recommendations include posterior STEMI as a formal STEMI equivalent, but only officially by 0.5
An undergraduate (not yet in medical school) who works as an ED technician (records all EKGs, helps with procedures, takes vital signs) and who reads this blog regularly arrived at work and happened to glance down and see this previously recorded ECG on a table in the ED. It was recorded at 0530: What do you think?
In EM Cases' first ECG Cases blog we review 7 examples of ECGs of patients presenting to the ED with chest pain, who's ECG were read as normal by the computer. And guess what.they all show acute ischemia!
This case shows a CT image of subendocardial ischemia. However, there are also Q-waves inferiorly and the inferior T-waves are inverted, suggesting that this is an old MI with persistent ST elevation, or, alternatively, a subacute or partially reperfused, inferior STEMI. This is all but diagnostic of inferior-posterior STEMI.
There may be ischemia present, but it is not evident on the ECG. LVH and the diagnosis of STEMI - how should we apply the current guidelines? This one mimics inferior STEMI (Figure 4): Concentric LVH, NO wall motion abnormality Case 5. How about diagnosing anterior STEMI in the setting of LVH? All troponins were negative.
This was a machine read STEMI positive OMI. Readers of this blog can easily appreciate the hyperacute T waves in the precordium, clearest in V1-V4. In this patient's case, the RV ischemia manifested as dramatic anterior hyperacute T waves. This degree of STE is a bit atypical for LAD ischemia. His ECG is shown below.
This study shows that for a transient STEMI ("complete normalization of ST segments"), it is not unequivocally necessary to activate the cath lab emergently. This might extend to Wellens' syndrome, which is really and transient STEMI in which the ST Elevation is not recorded. See more cases of Transient STEMI here: [link]
This certainly looks like an anterior STEMI (proximal LAD occlusion), with STE and hyperacute T-waves (HATW) in V2-V6 and I and aVL. This rules out subendocardial ischemia and is diagnostic of posterior OMI. How do you explain the anterior STEMI(+)OMI immediately after ROSC evolving into posterior OMI 30 minutes later?
The fact that R waves 2 through 6 are junctional does make ischemia more difficult to interpret -- but not impossible. Back to the assessment of ischemia: Returning to the ECG, the leads that catch my eye first are -- I, II, V4, V5, V6. For national registry purposes, this will be incorrectly classified as a STEMI.) < 0.049).
See my formula for differentiating anterior LV aneurysm (that is to say, persistent ST elevation after old MI) from acute anterior STEMI. Here is a link to a blog post with the formula , which we have recently validated and will publish. Both support acute anterior STEMI. As for thrombolytics, that is a bit riskier. 3.0 = 0.50
He had an immediate ED ECG: There is artifact, but the findings appear to be largely gone now The diagnosis is acute MI, but not STEMI. There is about 1 mm of STE in aVR I con sidered but rejected subendocardial ischemia. Is it subendocardial ischemia, or inferior MI? Here is his prehospital ECG: Diagnosis?
Important point: when there is diffuse subendocardial ischemia but no OMI, a wall motion abnormality will not necessarily be present. They agreed ischemia was likely in the setting of demand given DKA and infection. That this is all demand ischemia is unlikely. Lung exam showed diffuse B lines bilaterally. Aslanger's pattern.
This ECG is diagnostic of anterior STEMI. This is likely because 1) the ischemia to the inferior wall was only partial and 2) it reperfused quickly. The QRS is at least as important as the ST segment in diagnosing STEMI It has been constant since then. He looked ill and diaphoretic. BP was 160. Lessons: 1.
He was rushed by residents into our critical care room with a diagnosis of STEMI, and they handed me this ECG: There is sinus tachycardia with ST elevation in II, III, and aVF, as well as V4-V6. At first glance, it seems the patient is having a STEMI. ACS and STEMI generally do not cause tachycardia unless there is cardiogenic shock.
Dr. Smith’s ECG Blog has published a growing list of over 40 cases of ECGs falsely labeled ‘normal’ by the computer which are diagnostic of Occlusion MI, and Smith et al. Smith’s ECG Blog has published a growing list of over 40 cases of ECGs falsely labeled ‘normal’ by the computer which are diagnostic of Occlusion MI, and Smith et al.
Methods and Results Patients with confirmed ST elevation myocardial infarction (STEMI) treated by emergency medical services were included in this retrospective cohort analysis of the AVOID study. Greater severity of chest pain is presumed to be associated with a stronger likelihood of a true positive STEMI diagnosis. years old ± 13.7
Acute Q waves are a marker of severe ischemia and a predictor for delayed reperfusion. This patient could have very easily been overlooked, both because the ECG was STEMI negative and because the Q waves were attributed to an “old infarct”. Fortunately, Dr. Cho was not looking for STEMI ECG criteria but for an acute coronary occlusion.
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