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Date: November 22, 2023 Reference: Stopyra et al. Delayed First Medical Contact to Reperfusion Time Increases Mortality in Rural EMS Patients with STEMI. Date: November 22, 2023 Reference: Stopyra et al. Delayed First Medical Contact to Reperfusion Time Increases Mortality in Rural EMS Patients with STEMI.
A 60 yo with 2 previous inferior (RCA) STEMIs, stented, called 911 for one hour of chest pain. Here is his most recent previous ECG: This was recorded after intervention for inferior STEMI (with massive ST Elevation, see below), and shows inferior Q-waves with T-wave inversion typical of completed inferior OMI. ng/mL (quite large).
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]
So while there’s no diagnostic STEMI criteria, there are multiple ischemic abnormalities in 11/12 leads involving QRS, ST and T waves, which are diagnostic of a proximal LAD occlusion. First trop was 7,000ng/L (normal 25% of ‘Non-STEMI’ patients with delayed angiography have the exact same pathology of acute coronary occlusion.
Cath lab declined as it is not a STEMI." And now this finding is even formally endorsed as a "STEMI equivalent" in the 2022 ACC guidelines!!! Another myocardial wall is sacrificed at the altar of the STEMI/NonSTEMI mindset. de Winter et al in N Engl J Med 359:2071-2073, 2008. Cath attending is aware. Abstract 556.
Now lets walk through them quickly: Ho et al (4) looked at termination of VT in 15 min or hemodynamic deterioration. Gorgels et al (5) looked at procainamide vs lidocaine and again and primary outcome was VTach termination. Manz et al (6) looked at ajmaline vs lidocaine for the termination of VT. and Komura et al.,
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]
They wanted to know if I would like them to activate the outside hospital's "STEMI alert." But of course, this is not a STEMI by definition as it does not meet STEMI criteria. The STEMI guidelines do state that hyperacute T-waves "may indicate early acute myocardial infarction" but do not discuss it as a "STEMI equivalent."
Many conditions outside of acute coronary syndrome (ACS) mimic ST-elevation myocardial infarction (STEMI), but only a handful of cases have reported ST-elevations (STE) in the setting of pancreatic inflammation where underlying ACS was excluded. 2 Proposed hypothesis as described by Hsu et al., Yu ES, Lange JJ, Broor A, et al.
Date: September 8th, 2021 Reference: Desch et al. Date: September 8th, 2021 Reference: Desch et al. Defibrillation is the treatment of choice in these cases but does not often result in sustained ROSC ( Kudenchuk et al 2006). The TOMAHAWK Investigators. first appeared on The Skeptics Guide to Emergency Medicine.
This was a machine read STEMI positive OMI. 118.007305) from Heitner et al. , The meaning of this quote is that at times, something as obvious as the dramatic anterior lead ST elevation that we see in today's tracing is not the result of an acute LAD STEMI. His ECG is shown below. Pretty obvious anterior current of injury.
So this NSTEMI was likely a STEMI(-)OMI with delayed reperfusion. The patient was admitted as ‘NSTEMI’ which is supposed to represent a non-occlusive MI, but the underlying pathophysiology is analogous to a transient STEMI. Deutch et al. Fortunately the patient did not reocclude while awaiting the angiogram.
Their OMI Manifesto details how use of standard STEMI criteria results in an unacceptable level of inaccuracy, in which an estimated 25-30% of acute coronary occlusions are missed! The article by Aslanger, Smith et al that is featured above in today’s post has just been published.
There’s inferior ST depression which is reciprocal to subtle lateral convex ST elevation, and the precordial T waves are subtly hyperacute – all concerning for STEMI(-)OMI of proximal LAD. There’s ST elevation I/aVL/V2 that meet STEMI criteria. This is obvious STEMI(+)OMI of proximal LAD. Non-STEMI or STEMI(-)OMI?
The latest is Langlois-Carbonneau et al. If we took this as the gold standard, we would conclude that the computer interpretation was safe and accurate at least accurate enough to not miss STEMI, and that physicians should not be interrupted to interpret it, because there would be no change in patient management.
Date: January 28th, 2019 Reference: Chu DK et al. Date: January 28th, 2019 Reference: Chu DK et al. In the 2015 AVOID study there was some suggestion of increased MI size in the group of STEMI patients that received oxygen at 8 L/min compared to a room air control group. Reference: Chu DK et al. The Lancet 2018.
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. This is diagnostic of LAD occlusion but is equivocal for STEMI criteria and was missed (and both labeled ‘normal’ by final cardiology interpretation).
Lindahl et al. From Gue at al. 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. References: 1.
Unknown algorithm The Queen gets it right Case 4 How unreliable are computer algorithms in the Diagnosis of STEMI? The patient's prehospital ECG showed that there was massive STEMI and these are hyperacute T-waves "on the way down" as they normalize. Pain was resolving. Diagnosed as Normal by the computer. Troponin negative.
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.
Date: February 1, 2023 Reference: Wolfrum et al. Date: February 1, 2023 Reference: Wolfrum et al. A post-arrest ECG doesn’t show any signs of STEMI. Temperature Control After In-Hospital Cardiac Arrest: A Randomized Clinical Trial. Circulation. first appeared on The Skeptics Guide to Emergency Medicine. Circulation.
A prehospital STEMI activation was transmitted to the closest PCI center, and 324mg ASA was administered. The attending crews were concerned for an ACS-equivalent of LAD occlusion and initiated a prehospital STEMI activation to the closest PCI center. As the conversation progressed, another ECG spontaneously printed. 2] Driver, B.
This worried the crew of potential acute coronary syndrome and STEMI was activated pre-hospital. As it currently stands, an ST/S ratio >15% should raise awareness for new anterior STEMI. Smith comment : V5 and V6 are excessively discordant!!!! Here are two examples of HATW’s in the setting of confirmed LVH. Josephson, M. 40; 1234-1241.
Echo on the day after admission showed EF of 30-35% and antero-apical wall akinesis with an LV thrombus [these frequently form in complete or near complete (no early reperfusion) anterior STEMI because of akinesis/stasis] 2 more days later, this was recorded: ST elevation is still present. Claeys MJ, Bosmans J, Veenstra L, et al.
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. Herzog et al. Khan et al. Circulation 2007 2.
Notice on the right side of the image how the algorithm correctly measures STE sufficient in V1 and V2 to meet STEMI criteria in a man older than age 40. As most would agree, this ECG shows highly specific findings of anterolateral OMI, even with STEMI criteria in this case. Thus, this is obvious STEMI(+) OMI until proven otherwise.
Here it is: Obvious Inferior Posterior STEMI (+) OMI. Initial troponin was: 3 ng/L We showed that the first troponin in acute STEMI is often negative in at least 27%. Aside on ECG Research: 20% of Definite diagnostic STEMI (Cox et al.) The cath lab was activated prehospital But imagine if the patient had walked in.
The prehospital and ED computer interpretation was inferior STEMI: There’s normal sinus rhythm, first degree AV block and RBBB, normal axis and normal voltages. The paramedic notes called STEMI into question: “EMS disagree with monitor for STEMI callout. Vitals were normal except for oxygen saturation of 94%. Vitals were normal.
The conventional machine algorithm interpreted this ECG as STEMI. See this post of RV MI with both McConnell sign and "D" sign: Inferior and Posterior STEMI. She was out walking her dog when she developed sudden dizziness and light-headedness. When EMS found her, she was dyspneic and diaphoretic.
The criteria of Armstrong et al. would require the ST/S ratio to be 25% for diagnosis of STEMI in LVH. The physician was concerned about STEMI, but also worried that she was overreacting, with the potential that LVH was producing a "STEMI-mimic." Can you diagnose an ACO (STEMI) when you also have LVH? J Emerg Med.
Quiz : What percent of full blown STEMI have an open artery with normal flow at angiogram? It too is "normal" and you decide that this is not OMI or STEMI and you just decide to get troponins. Jesse McLaren et al. I would expect that a stent would be placed. In the meantime, a lot of myocardium is lost.
There is mixed overlap of ST-segment elevation (STE), ST-segment depression (STD), Hyperacute T waves (HATW), and deWinter pattern (which the ACC regards as a STEMI-equivalent but is better suited under the blanket of OMI). link] [1] Zachary et al. Western Journal of Emergency Medicine, 18 (4), 752-760. [2] 2] Costanzo, L. Physiology.
The Queen of Hearts agrees: Here the Queen explains why: However, it was not interpreted correctly by the providers: ED interpretation of ECG: "paced rhythm, LBBB but no STEMI pattern." Most large STEMI have peak troponin I in the 20.0 There are hyperacute T-waves in V5 and V6. Next trop in AM. Peak trop 257.97 ng/mL - 80.0
Figure 1-1 My colleague, a faithful student of ECG interpretation, handed me the tracing and said that it warranted STEMI activation because of apparent terminal QRS distortion (TQRSD) in V2. ASA 324mg was administered while a STEMI activation was simultaneously transmitted to the nearest PCI center. 4] Baranchuk, A, et al.
A Short Comment on PIRP and T Waves: Oliva et al found a strong association of myocardial rupture with postinfarction regional pericarditis. 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.
I believe there is not quite enough STE for formal STEMI criteria, but some might measure 1.0 mm of STE in II and III, or III and aVF, or V4 and V5, so some might say it fulfills STEMI criteria (remember, the interrater reliability of STEMI criteria is poor as shown in references below): McCabe et al. Carley et al.
The precordial ST-depression pattern on this ECG (and in this clinical setting) should immediately raise suspicion of Posterior STEMI! Posterior STEMI occurs in approximately 15-20% of acute MI, but the vast majority of the time it is seen in conjunction with inferior (Infero-Posterior) or lateral (Postero-Lateral) STEMI (1).
Validation of the Modified Sgarbossa Rule for Diagnosis of STEMI in the Presence of Left Bundle Branch Block. Meyers HP et al. Pendell is the lead author on our Modified Sgarbossa Criteria Validation Study. Limkakeng AT. Theiling BJ. American Heart Journal 170(6):1255-1264; December 2015. 0 0 1 41 238 MMRF 1 1 278 14.0
His ECG was repeated at this point: This shows a well developed anterior STEMI. To not see these findings is very common, and this patient would be given the diagnosis of NonSTEMI, with subsequent development of STEMI. It is not a missed STEMI, but it is a missed coronary occlusion. Fesmire et al. Marti D et al.
Precordial ST depression may be subendocardial ischemia or posterior STEMI. If you thought it might be a posterior STEMI, then you might have ordered a posterior ECG [change leads V4-V6 around to the back (V7-V9)]. So there was 3-vessel disease, but with an acute posterior STEMI. Conversely, Matetzky et al.
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%
Here is his ED ECG at triage: Obvious high lateral OMI that does not quite meet STEMI criteria. Studies such as those by Moise et al 14 and Ellis et al 39 have shown that the relative risk of developing an acute myocardial infarction in the territory supplied by an artery with a 70%. He was started on nitro gtt.
Patient still not having chest pain however this is more concerning for OMI/STEMI. Wellens' syndrome is a syndrome of Transient OMI (old terminology would be transient STEMI). As far as I can tell, there is only one randomized trial of immediate vs. delayed intervention for transient STEMI. Lemkes JS, et al.
But because there was no new ST elevation, the ECG was signed off as “STEMI negative” and the patient waited to be seen. But the ECG still doesn’t meet STEMI criteria. It was therefore interpreted as “no STEMI” and the patient was treated with dual anti-platelets and referred to cardiology as “NSTEMI.” the cardiologist 5.
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