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Cardiogenic shock (CS)is the most feared event following STEMI. We tend to perceive CS as an exclusive complication of STEMI. The incidence is half of that of STEMI, i.e., 2.5-5%. might show little elevation with considerable overlap of left main STEMI vs NSTEMI ) 2.Onset ACS pathophysiology is not that simple.
This was a machine read STEMI positive OMI. 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. Written by Willy Frick A 50 year old man with no medical history presented with acute onset substernal chest pain. His ECG is shown below.
You can subscribe for news and early access (via participating in our studies) to the Queen of Hearts here: [link] queen-form This EMS ECG was transmitted to the nearby Emergency Department where it was remotely reviewed by a physician, who interpreted it as normal, or at least without any features of ischemia or STEMI.
4,5] We have now formally studied this question: Emergency department Code STEMI patients with initial electrocardiogram labeled ‘normal’ by computer interpretation: a 7-year retrospective review.[6] have published a number of warnings about the previous reassuring studies.[4,5]
Written by Bobby Nicholson What do you think of this “STEMI”? or basilar ischemia. Second, although there is a lot of ST Elevation which meets STEMI criteria, especially in V3-4, the ST segment is extremely upwardly concave with very large J-waves (J-point notching). EKG on arrival to the ED is shown below: What do you think?
The ECG shows obvious STEMI(+) OMI due to probable proximal LAD occlusion. There is no definite evidence of acute ischemia. (ie, Simply stated — t he patient was having recurrent PMVT without Q Tc prolongation, and without evidence of ongoing transmural ischemia. ( The below ECG was recorded.
A prior ECG was available for comparison: Normal One might be tempted to interpret the ST depression as ischemia, but as Smith says, "when the QT is impossibly long, think of hypokalemia and a U-wave rather than T-wave." Is it STEMI? Instead — it commonly reflects ischemia from severe underlying coronary disease.
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. His response: “subendocardial ischemia. Anything more on history? POCUS will be helpful.”
Step 1 to missing posterior MI is relying on the STEMI criteria. A prospective validation of STEMI criteria based on the first ED ECG found it was only 21% sensitive for Occlusion MI, and disproportionately missed inferoposterior OMI.[1] But it is still STEMI negative. A 15 lead ECG was done (below). In a study last year, 14.4%
Subendocardial Ischemia from another Cause ( ie, sustained tachyarrhythmia; cardiac arrest; shock or profound hypotension; GI bleeding; anemia; "sick patient" , etc. ). To EMPHASIZE: This pattern of diffuse Subendocardial Ischemia does not suggest acute coronary occlusion ( ie, it is not the pattern of an acute MI ).
In any case, the ECG is diagnostic of severe ischemia and probably OMI. So this could be myocarditis but in my opinion needs an angiogram before making that diagnosis. == Dr. Nossen Comment/Interpretation: Evaluation of ischemia on an ECG can be very challenging. Concordant STE of 1 mm in just one lead or 2a.
A prehospital “STEMI” activation was called on a 75 year old male ( Patient 1 ) with a history of hyperlipidemia and LAD and Cx OMI with stent placement. Whether these EKGs show myocarditis, a normal variant, or something else, they are overall not typical of transmural ischemia of the anterior or high lateral walls.
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?
When the ST vector is primarily posterior, the diagnosis is usually posterior STEMI. Contrary to what Ken stated, the ST vector remains mostly posterior __ What about subendocardial ischemia? Subendocardial ischemia results in ST depression, but unfortunately, and rather mysteriously, it does not localize to the ischemic wall.
Here is the EMS ECG: Obviously massive diffuse subendocardial ischemia, with profound STD and STE in aVR Of course this pattern is most often seen from etoliogies other than ACS. The ECG only tells you there is ischemia, not the etiology of it. Nevertheless, the clinical situation made other etiologies unlikely.
[link] deWinter first reported his unique characteristics of LAD occlusion in 2008, and since the respective ECG changes do not fit the conventional STEMI paradigm (as he even stated – “instead of signature ST-segment elevation” ….) it has been subsequently deemed a STEMI-equivalent.
So Shark Fin really is just a dramatic representation of STEMI, and can be in any coronary distribution. So this is STEMI, right? Our chief of cardiology, Gautam Shroff, interprets it differently and thinks this is indeed ischemia. It is often confused with a wide QRS due to conditions such as hyperkalemia. Which artery?
If it is STEMI, it would have to be RBBB with STEMI. Followup ECG: No Change Absence of evolution is the best evidence against ischemia as the etiology. I was taught that the tell-tale sign of ischemia vs an electrical abnormality was in the hx, i.e. chest pain for the ischemia and potential syncope for brugada.
QOH versions 1 and 2 both say Not OMI, with high confidence, without any clinical context, despite the abnormal STE meeting STEMI criteria. That said — I did not interpret these differences as the result of acute ischemia. Of note, there is arguably terminal QRS distortion in V4-V6. Pericarditis maybe."
This blog post reviews the basics for predicting the " C ulprit" A rtery — as well as the importance of the term, " O MI" ( = O cclusion-based MI ) as an improvement from the outdated STEMI paradigm. ECG Blog #271 — Reviews determination of the ST segment baseline ( with discussion of the entity of diffuse Subendocardial Ischemia).
There is broad subendocardial ischemia as demonstrated by STE aVR with concomitant STD that almost appears appropriately maximal in Leads II and V5. There is LBBB-like morphology with persistent patterns of subendocardial ischemia. This worried the crew of potential acute coronary syndrome and STEMI was activated pre-hospital.
Here, I do not see OMI (although the ECG is falsely STEMI positive with just over 1 mm STE in V1 and about 2.5 In the days before I learned to look for OMI, back when I was counting ST elevation boxes, I used to save ischemia for last.) I interpret tracings systematically in "real time" ( including my assessment for acute ischemia ).
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. JAMA Intern Med 2019 9. Yazdi D, Sharim J.
When “spot diagnosing” precordial ST-depression I instinctively evaluate aVR for any corresponding ST-elevation to see if an emerging pattern of broad subendocardial ischemia can be appreciated, in which the ST-depression should be otherwise global and demonstrably maximal in Leads II and V5. However, in this context (i.e. is present.
Inferior ST Depression does NOT mean there is inferior subendocardial ischemia; it is generally reciprocal to high lateral (aVL) subepicardial ischemia (OMI/STEMI) == MY Comment by K EN G RAUER, MD ( 2/10/2023 ): == There are certain patterns in ECG interpretation that experienced providers are able to immediately recognize.
The attending crews were concerned for SVT with corresponding ischemic hyperacute T waves (HATW) and subsequently activated STEMI pre-hospital. Then, three minutes later… Crews activated STEMI as she deteriorated into PEA arrest. Chapter 6: Introduction to Myocardial Ischemia and Infarction. Wolters-Kluwer: Philadelphia, PA. [2]
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.
Part of the ST depression with deep T wave inversion in the lateral chest leads clearly reflects LV "strain" from the marked LVH — but despite the very large QRS amplitudes, this ST-T wave appearance looks disproportionate, suggesting at least a component of ischemia. Then there is the significant ST elevation we see in lead V1.
This strongly suggests reperfusing RCA ischemia. Troponins, echocardiogram An echocardiogram showed inferobasilar hypokinesis, further supporting a diagnosis of regional ischemia , likely of the area supplied by the RCA. A recent study found that SCAD causes almost 20% of STEMI in young women. JACC 2019 Sep 10;74(10):1290-1300.
It does not usually represent subendocardial ischemia, but rather it is usually reciprocal ST depression, reciprocal to inferior ST elevation. Still does not meet STEMI criteria, but it is an obvious OMI And then another one became more obvious: Cath lab was activated and a 100% RCA occlusion was found. (But
There is STE that does not meet STEMI criteria in V1-V6. This patient's ischemia was so brief that it did not cause any myocardial stunning. This was mistaken by the treating physicians for ST depression initially. Precordial leads: What do you think? This is diagnostic of LAD OMI. These are hyperacute T-waves.
Does this mean that the ST depression in V3 represents "anterior" subendocardial ischemia, and not posterior OMI? This is most consistent with ischemia/infarction in the distribution of the left circumflex coronary artery. non-occlusive ischemia) 2. Thus, they have much less voltage. They have ZERO ST Elevation.
The morphology of STE is not diagnostic of being due to acute transmural ischemia. This one likely does meet STEMI criteria in II, III, and aVF. The development of an inferior-posterior STEMI, from prehospital to hospital Inferior hyperacute T-waves. Criteria for a STEMI are definitely not met in ECG #1. What happened?
In other words, the inferior ST segments in the first ECG show more straightening which is more concerning for ischemia. In this context, patient pain free — post-PCI and with the previous ECGs in mind— the large inferior T waves represent reciprocal change from lateral reperfusion T waves and are not hyperacute T waves of ischemia.
The STEMI criteria in normal conduction are only 75% sensitive for OMI!! A Fascinating Demonstration of ST/S Ratio in LBBB and Resolving LAD Ischemia Chest pain with New LBBB: It helps to actually measure the ST/S ratio == Comment by K EN G RAUER, MD ( 4/7/2019 ): == Hindsight is 100% in the retrospectoscope.
The only time you see this without ischemia is when there is an abnormal QRS, such as LVH, LBBB, LV aneurysm (old MI with persistent STE) or WPW." Here is the patient's troponin I profile: These were interpreted as due to demand ischemia, or type II MI. ng/mL is seldom a result of demand ischemia (type 2 MI). First was 2.9
These findings are concerning for inferior wall ischemia with possible posterior wall involvement. The morphology in V2 is also concerning and it appears that the ST segment is being pushed down, as in ST depression. In lead III there is the tiniest possible amount of STE which is difficult to measure due to the very low-voltage.
This ECG clearly meets STEMI criteria by the way, regardless of age or gender. Weren't you taught that "new tall T wave in V1" is concerning for ischemia, and so this is the opposite? This is a high troponin (most STEMI are above 10 ng/mL for troponin I). There is no STE or STD in III an aVF. Leads V4-V6 show new loss of S-wave.
PCI mid LCx So this is an OMI (Occlusion Myocardial Infarction), but not a STEMI Echo: Decreased left ventricular systolic performance, mild/moderate. This figure comes from the Diamond T study (all type 1 MI were NSTEMI, not STEMI): Notice that the 6 hour value (far right) is very low for type 2 MI. Angiogram: LM 30% ostial.
2 days later This is a typical LVH pattern, without ischemia Patient underwent 4 vessel CABG. For more on T-QRS-D — Please see My Comment at the bottom of the page in the November 14, 2019 post in Dr. Smith's ECG Blog ). which would suggest reduced rates of major adverse cardiac events with coronary artery bypass grafting."
Figure-4: ECG findings to look for when your patient with new-onset cardiac symptoms does not manifest STEMI-criteria ST elevation on ECG. For my clarifying Figure illustrating T-QRS-D ( 2nd bullet ) — See My Comment at the bottom of the page in Dr. Smith’s November 14, 2019 post. = ECG Blog #205 = The Systematic Approach I favor.
mmm ECG Blog #193 — Reviews the concept of why the term “OMI” ( = O cclusion-based MI ) should replace the more familiar term STEMI — and — reviews the basics on how to predict the " culprit " artery. ECG Blog #271 — Reviews determination of the ST segment baseline ( with discussion of the entity of diffuse Subendocardial Ischemia).
This suggests further severe ischemia. STEMI MINOCA versus NSTEMI MINOCA STEMI occurs in the presence of transmural ischaemia due to transient or persistent complete occlusion of the infarct-related coronary artery. This has resulted in an under-representation of STEMI MINOCA patients in the literature. From Gue at al.
ECG Blog #193 — Reviews the concept of why the term “OMI” ( = O cclusion-based MI ) should replace the more familiar term STEMI — and — reviews the basics on how to predict the " culprit " artery. The January 9, 2019 post in Dr. Smith's ECG Blog ( Please scroll down to the bottom of the page to see My Comment ).
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