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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.
Background: Primary PCI is the recommended reperfusion strategy in patients with STEMI and should be initiated within 2 hours after first medical contact. Paper: Van de Werf, F et al. In non-PCI-capable hospitals this goal is not always achievable due to delays in transfer. Primary PCI: 95.7% Primary PCI: 95.7% Primary PCI: 78.4%
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.
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]
I sent this to the Queen of Hearts So the ECG is both STEMI negative and has no subtle diagnostic signs of occlusion. Similarly, if a patient with known CAD presents with refractory ischemic chest pain, the ECG barely matters: the pre-test likelihood of acute coronary occlusion is so high that they need an emergent angiogram.
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). Acute coronary syndrome (ACS) is responsible for the majority (60%) of all OHCAs in patients.
[display_podcast] Date: October 19th, 2017 Reference: Hofmann et al. display_podcast] Date: October 19th, 2017 Reference: Hofmann et al. The ECG shows an inferior ST-Elevated Myocardial Infarction (STEMI). A systematic review by Wijesinge et al from 2009 found only two randomized control trials looking at supplemental oxygen.
The latest is Langlois-Carbonneau et al. But like many similar studies, the study was small (one year at one centre with no indication of the incidence of acute coronary occlusion), and it used as the gold standard the final cardiologist interpretation of the ECG - not the patient outcome!
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. Do NOT give it unless you are committed to the cath lab!! Cath attending is aware. It is a mass delusion.
Additional architectural changes include systolic anterior motion of the mitral valve, endothelial dysfunction at the level of the coronary arterial bed, and ventricular diastolic dysfunction. This worried the crew of potential acute coronary syndrome and STEMI was activated pre-hospital. It is spread to V2 and V3.
The proof of this is that only 5% of patients enrolled had acute coronary occlusion. COACT: The COACT trial was fatally flawed, and because of it, many cardiologists are convinced that if there are no STEMI criteria, the patient does not need to go to the cath lab. Lemkes JS, Janssens GN, van der Hoeven NW, et al. 5% vs. 58%!!
Old ‘NSTEMI’ A history of coronary artery disease and a stent to the same territory further increases pre-test likelihood of acute coronary occlusion, including in-stent thrombosis. So this NSTEMI was likely a STEMI(-)OMI with delayed reperfusion. Deutch et al.
A prehospital STEMI activation was transmitted to the closest PCI center, and 324mg ASA was administered. One cannot rely on this feature as a means of detecting changes – subtle, or dramatic – for volatile occlusive coronary thrombus. It’s important to stress the presence of a normal QRS (i.e., The pathology is now painfully evident.
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.
BP 142/100 HR 90 RR 16 (BBS CTA) SpO2 99 (RA) Dstick 110 My colleagues noted the ST-depression in the respective leads, as well, and STEMI activated to the nearest PCI center. 1] Here is the admitting ED ECG after cancellation of Code STEMI. Cardiology admitted him for observation with plans for next-day coronary angiogram.
There is appreciable STE aVR with near-global STD that appropriately maximizes in Leads II and V5, and thus suggesting a circumstance of generic, diffusely populated, circumferential subendocardial ischemia versus occlusive coronary thrombus. [1] STEMI was activated and the patient went to Cath on arrival. link] [1] Mirand, D.
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. Thanks in part to rapid bedside diagnosis, the patient was able to avoid emergent coronary angiography. When EMS found her, she was dyspneic and diaphoretic.
Below is the version standardized by PM Cardio app Meyers interpretation: Findings are specific for posterior (and also likely inferior) wall transmural acute infarction, most likely due to acute coronary occlusion (OMI). Smith Comment: Is is common for the artery to be open at angiogram in OMI, including full STEMI.
Zeymer HT et al. References: Zeymer HT et al. The benefits of this strategy may be outweighed by the risk of the device-related complications (i.e. bleeding, stroke, limb ischemia, and hemolysis). The evidence for this practice has been sparse until now. Extracorporeal Life Support in Infarct-Related Cardiogenic Shock. Control: 53.4%
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.
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? Widimsky P et al.
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). A comparison of electrocardiographic changes during reperfusion of acute myocardial infarction by thrombolysis or percutaneous transluminal coronary angioplasty.
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.
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?
You can see how V1, V2, aVR, and V4R would have ST elevation in either a right ventricular STEMI or with a septal STEMI, and how lateral leads, and even posterior leads, would have reciprocal ST depression. In a 1999 study by Engelen et al. of patients with anterior STEMI, ST elevation of greater than or equal to 3.0
for those of you who do not do Emergency Medicine, ECGs are handed to us without any clinical context) The ECG was read simply as "No STEMI." In fact, Kosuge et al. Electrocardiographic Differentiation Between Acute Pulmonary Embolism and Acute Coronary Syndromes on the Basis of Negative T Waves - ScienceDirect. Stein et al.
It should be emphasized here that this is a presentation of high-pretest probability for Acute Coronary Syndrome (ACS). 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).
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.
Thus, this is both an anterior and inferior STEMI. How old is this antero-inferior STEMI? Although acute anterior STEMI frequently has narrow QR-waves within one hour of onset (1. Raitt et al.) [and Armstrong et al.)], the presence of such well developed anterior Q-wave suggests completed transmural STEMI.
The receiving emergency physician consulted with interventional cardiology who stated there was no STEMI. Serial ECGs enhance the diagnosis of acute coronary syndrome. Bigger et al. Is there STEMI? Sadowski ZP, Alexander JH, Skrabucha B, et al. The patient continued having chest pain. Leave it alone. Moffat, M.
The ECG shows obvious STEMI(+) OMI due to probable proximal LAD occlusion. It shows a proximal LAD occlusion, in conjunction with a subtotally occluded LMCA ( Left Main Coronary Artery ). The patient in today’s case is a previously healthy 40-something male who contacted EMS due to acute onset crushing chest pain.
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.) have perfect coronary flow by the time of angiogram. Clinical history is needed.
Thus, this is BOTH an anterior and inferior STEMI in the setting of RBBB. How old is this antero-inferior STEMI? Although acute anterior STEMI frequently has narrow QR-waves within one hour of onset (1. Raitt et al.), Raitt et al.), Armstrong et al.), 3) Oliva et al. (4) Armstrong PW et al.
This ECG was read as “No STEMI” with no prior available for comparison. It is true this ECG does not meet STEMI criteria (there is 1.0 Armstrong et al. The patient has also developed sinus bradycardia, which may result from right coronary artery ischemia to the SA node. What do you think? mm STE in III, and possibly 0.5
The commonest causes of MINOCA include: atherosclerotic causes such as plaque rupture or erosion with spontaneous thrombolysis, and non-atherosclerotic causes such as coronary vasospasm (sometimes called variant angina or Prinzmetal's angina), coronary embolism or thrombosis, possibly microvascular dysfunction. This is not the case.
The attending crews were concerned for SVT with corresponding ischemic hyperacute T waves (HATW) and subsequently activated STEMI pre-hospital. Cardiology was consulted, who advised to surveil a metabolic process as this did not strike them as acute coronary syndrome. Closer inspection will show that it is Sinus, after all.
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. Coronaries were normal, as was serial troponin. Vitals were normal.
He reported a history of ischemic cardiomyopathy with coronary stent placement approximately 10 years prior, but could not recall the specific artery involved. ASA 324mg was administered while a STEMI activation was simultaneously transmitted to the nearest PCI center. 4] Baranchuk, A, et al. Attached is the first ECG.
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).
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.
Background: Historically, we have treated acute coronary syndrome with supplemental oxygen regardless of the patient ’ s oxygen saturation. More recent evidence, however, demonstrates that too much oxygen could be harmful ( AVOID Trial ) by causing coronary vasoconstriction and increasing oxidative stress. Low O2 protocol: 3.1%
You've read in my previous posts that I have a lot of evidence that Wellens' represents spontaneously reperfused STEMI in which the STEMI went unrecorded. New ST elevation diagnostic of STEMI [equation value = 25.3 Akkerhuis KM, et al. Gottlieb SO, et al. Jernberg T, et al. Patel DJ, et al.
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