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Recall from this post referencing this study that "reciprocal STD in aVL is highly sensitive for inferior OMI (far better than STEMI criteria) and excludes pericarditis, but is not specific for OMI." Case continued She was loaded with aspirin 325 mg, and repeat troponin drawn around the time of EKG 1 resulted at 267 ng/L. At midnight.
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. Here is lead I from ECGs 1 and 2 shown side-by-side to highlight the change in axis from borderline right to completely normal. Her ECG is shown below: What do you think?
link] A 62 year old man with a history of hypertension, type 2 diabetes mellitus, and carotid artery stenosis called 911 at 9:30 in the morning with complaint of chest pain. Challenge QUESTION: The relative change in T-QRS-D is not the only thing that changes during period of time that passed between recording of the 2 ECGs shown in Figure-1.
== MY Comment , by K EN G RAUER, MD ( 8/30 /2024 ): == I was sent the ECG shown in Figure-1 — knowing only that the patient was being seen in the ED ( E mergency D epartment ). Figure-1: The initial ECG in today's case. After seeing ECG #2 — Can you explain: i ) Why no negative P wave was seen in lead V1 of ECG #1? —
A prior ECG from 1 month ago was available: The presentation ECG was interpreted as STEMI and the patient was transferred emergently to the nearest PCI center. Patients that develop a Type 1 pattern without any precipitating or provoking factors have a risk of SCD of 0.5-0.8% per year incidence of SCD in this cohort [1].
Pain improved to 1/10 after EMS administers 324 mg aspirin and the following EKG is obtained at triage. 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." found normal ECGs in only 3 of 50 patients with massive PE, and 9 of 40 with submassive PE.
Post cath ECG: Now there are hyperacute T-waves again, and recurrent ST depression in V2 This ECG would normally diagnostic of OMI until proven otherwise No further troponins were measured, but it looks like there is recurrent OMI Next day: A CT Coronary Angiogram was done (CTCA) CARDIAC MORPHOLOGY AND FUNCTION: 1. IMPRESSION: 1.
Furthermore, the term "STEMI equivalent" has no reliable or definable meaning except between two practitioners who both agree on the list of entities that they believe are STEMI equivalents and can agree on how to identify it. Obvious inferoposterior STEMI. J ACC 61(4):e78-140; page e83.
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. Armstrong et al.)], the presence of such well developed anterior Q-wave suggests completed transmural STEMI. Could it be acute (vs.
Two recent interventions have proven in randomized trials to improve neurologic survival in cardiac arrest: 1) the combination of the ResQPod and the ResQPump (suction device for compression-decompression CPR -- Lancet 2011 ) and 2) Dual Sequential defibrillation. Figure-1: The initial ECG in today's case — obtained after ROSC.
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. the presence of such well developed, wide, anterior Q-wave suggests completed transmural STEMI. Lessons : 1.
Guidelines recommend the use of validated risk models to estimate the risk of acute myocardial infarction , 30-days and 1-year mortality in patients with NSTE-ACS. TIMI Risk Scores for NSTE-ACS (NSTEMI, UA) and STE-ACS ( STEMI ) can be calculated below. TIMI, GRACE and PURSUIT are such risk models. Circulation.
There is an obvious inferior posterior STEMI(+) OMI. We recorded an ECG in which V1-V3 were put in the position of V4R-V6R, and V4-6 were placed in V7-9 to (academically) confirm posterior OMI. 1 mg of Atropine was given and the heart rate increased transiently to 60. What is the atrial activity? How would one tell? What to do?
Post Cath ECG: Obviously completing MI with LVA morphology, and STE that meets STEMI criteria (but pt is still diagnosed as "NSTEMI"). Day 12 ECG: FINAL DIAGNOSIS: "NSTEMI" Despite the fact that his day 4 ECG easily meets STEMI criteria, the patient is diagnosed as NSTEMI. No TIMI flow was listed in the report.
There is STE in III and aVF which does not meet STEMI criteria due to insufficient STE in lead aVF. The interventionalists insisted that the ECGs did not meet STEMI criteria and cancelled the activation, stating that they would consider urgent cath after further stabilization. This is an obvious inferoposterior OMI. mm STE with 9.5
He had episodes of chest pain off and on all night, until about 1 hour prior to arrival when the pain became constant, crushing, 10/10 chest pain that radiated to both arms. Barely any STE, and thus not meeting STEMI criteria. Only now that the patient has STEMI criteria is he allowed to go to the cath lab, at around 0530.
A 40-something male presented with dyspnea and left arm numbness, and perhaps some chest tightness, for 11/2 hours. This is all but diagnostic of STEMI, probably due to wraparound LAD The cath lab was activated. Here is his triage ECG: There is massive STE in V3-V6, and also STE in II, III, aVF. Why is this important?
Then, 1 hour before arrival, it recurred, again lasting 5 minutes. There is STE that does not meet STEMI criteria in V1-V6. For clarity — I’ve put the 2 pieces of the 1st ECG together, and I’ve relabeled the tracings ( Figure-1 ). Figure-1: The first 2 ECGs in this case ( See text ). It lasted 5 minutes then resolved.
Here it is: The computer reads STEMI What do you think? More from the medic: "LifePak 15 interpretation was STEMI. My response: "I think it is very worrisome for STEMI." It meets STEMI criteria even for a male under age 40, with STE 2.84 No history, meds, or risk factors. Pattern looked to be BER. mm in V2 and 4.08
There are two main etiologies of ischemic ST-depression: 1) subendocardial ischemia 2) reciprocal to ST-elevation in an opposite wall Here there are distinct R-waves with marked ST-depression throughout most of the precordium. But if there is none - then you are looking at least at an Isolated Posterior STEMI until proven otherwise.
The pattern of STE and STD reminded us of Brugada Type 1 morphology. Smith comment: 1) Brugada ECG may have ST shifts in limb leads as well as precordial leads. 2) The STE in V1 and V2 has an R'-wave and downsloping ST segments, very atypical for STEMI. per year incidence of SCD in this cohort [1]. Bicarb 20, Lactate 4.2,
As always, LAD OMI need not meet STEMI criteria and usually does NOT! Here are many examples which we have already posted: 5 of LVH mimicking Precordial Swirl 1 case (Case 6) of LVH mimicking precordial swirl, but it is actually LVH + posterior OMI 14 Cases (Cases 7-20) of OMI with Precordial Swirl First, 5 mimics: Case 1.
For clarity — I’ve put these 2 tracings together in Figure-1. Figure-1: The initial ED ECG ( = E CG # 1) — with comparison to the patient’s baseline ECG done 4 years earlier ( = E CG # 3). The ECG finding that I KNOW is real in ECG #1 is the mirror - image appearance of ST-T waves in leads III and aVL.
But these cases show the potential dangers of delayed recognition and treatment of inferior reperfusion Take away 1. Rather than using terms like “STEMI” and “Wellens”, it’s more helpful to describe the underlying pathology and ECG pattern pattern: Occlusion MI, and reperfusion T wave inversion 4. JAMA Intern Med 2019 9.
A "STEMI alert" was called and soon cancelled. Comment by K EN G RAUER, MD ( 3/1 /2023 ): = Today's case by Dr. Meyers serves as a reminder of the important clinical entity known as diffuse subendocardial ischemia. ST depression will not always be present in 9/12 leads — as is seen in Figure-1.
Here they are: Learning Points: 1. 7 These 3 studies, as well as 1 smaller meta-analysis, 6 and another small study, 8 make it clear that troponin is associated with increased severity and mortality in COVID when adjusted for multiple other variables. 12 All STEMI patients had very high cTn typical of STEMI (cTnT > 1.0
On review of systems the patient reported back pain for approximately 1 week which he was treating with NSAIDs with minimal relief. normal variant, not pericarditis) A Young Man with Sharp Chest pain (normal variant, not pericarditis) 24 yo woman with chest pain: Is this STEMI? 15-9/6/2017 ). Pericarditis?
mm of ST segment elevation, V2 and V3 have 1 mm of elevation, v4 has 2 mm of elevation and v5 around 1.5 Note 1: Levels were significantly lower in takotsubo that presented with T-wave inversion. Reference on Troponins: Xenogiannis I, Vemmou E, Nikolakopoulos I, et al. Learning Points: 1. What do you think? V1 has 0.5
It does not meet STEMI criteria. Obvious STEMI(+) OMI of inferior, posterior, and lateral walls, now with likely 2nd degree heart block type 1 (Wenckebach). Learning Points: We can find OMI on ECG much sooner than STEMI criteria in many cases, and of course many OMIs never meet STEMI criteria at all.
Despite the clinical context, Cardiology was consulted due to concerns for a "STEMI". Hyperkalemia mimics STEMI and OMI in many distributions, but probably the most common is the Brugada morphology in V1-V2 which mimics anterior OMI for those who cannot recognize the Brugada pattern. Limb lead reversal can be easily recognized.
Easy LINK — [link] — My New E CG P odcasts ( 5/28/2024 ): These podcasts are part of the Mayo Clinic Cardiovascular CME Podcasts Series ( "Making Waves" ) — hosted by Dr. Anthony Kashou. 2:25 — Dr. Grauer: The 1st Error : Too many clinicians in 2024 are still stuck in the outdated millimeter-based STEMI Paradigm”.
If you were thinking that this is not anterior OMI because there is no reciprocal ST depression , it is important to remember that half of anterior STEMI do NOT have any reciprocal ST depression. There are some unusual ECG findings in today's tracing ( that I labeled in Figure-1 ). Anterior OMI? Pericarditis?
Important Learning Point: "STEMI" is defined by millimeter criteria (1 mm in limb leads), which this does not meet. Therefore it is not a STEMI. But what we truly care about is coronary occlusion, for which STEMI is just a surrogate that is only about 75% sensitive for occlusion. Some are STEMI-equivalents.
Not quite a STEMI, but same effect.) There is ST elevation in V2-V4 that does not quite meet "STEMI criteria." That is a reasonable thought, but we have shown that if there is one lead of V1-V4 with a T/QRS ratio greater than 0.36, then it is STEMI, not LV aneurysm. Is this a transient STEMI? Learning Points: 1.
I was relieved to see this MRI result: MRI IMPRESSION 1) Mildly decreased LV function with no focal wall motion abnormalities. Learning Points: 1. Cases of acute MI that were initially misdiagnosed as myo- or peri-carditis: 24 yo woman with chest pain: Is this STEMI? BUT — “ Y a g otta b e t here”. Pericarditis?
Anterior STEMI? Regarding the History: It sounds from the History as if this patient has at least a significant component of EIA ( E xercise- I nduced A sthma ). Dr. T-wave inversions and dynamic ST elevation Tachycardia, hyperthyroid, and ST elevation. What is it? Activate the Cath Lab?
Angiogram showed a 99% left main thrombotic occlusion with TIMI-1 flow (this is considered "occlusion" even though there is some flow. not left main occlusion == MY Comment by K EN G RAUER, MD ( 1/16/2020 ): == I did not correctly identify the “culprit artery” in this case. Marked acute STEMI changes in no less than 4 lateral leads.
EMS recorded these prehospital ECGs: Time 0: In V2-V4, there is ST elevation that does not meet STEMI "criteria," of 1.5 If you use something like the HEART score: 1. E EKG: a negative ECG (score = 0) 3. She was having a transient STEMI, briefly. Learning Points : 1. She called 911. A Age: = 0 4. It was stented.
The neurologic section was divided into (1) brain oxygenation, perfusion, edema, and intracranial pressure (ICP); (2) seizures and the ictal-interictal continuum (IIC); and (3) sedation and analgesia. Authors state early cath may be of benefit in those with no STEMI, but much of the more recent literature suggests this is more controversial.
S-wave is in V2 = 17 mm S-wave V4 = 9 mm Total = 26 (not greater than 28), so not LVH by the new rule! But lead V2 has a worrisome amount of ST elevation, and in a chest pain patient, I would be worried about STEMI. For clarity — I’ve reproduced this ECG, to which I’ve made a few additions ( Figure-1 ). Peguero JG et al.
1 week later (about 1 week prior to the tamponade visit) she had a follow up outpatient visit and this ECG was recorded: Appears to show resolving findings. For an excellent review of the pathophysiological explanation of signs and symptoms associated with Pericardial Tamponade SEE this Review by Jensen et al in the e-Journal Card.
Even before we have clinical context, this ECG simply does not appear concerning for OMI, notwithstanding the machine's interpretation ** ** ACUTE MI / STEMI ** **. But in the world of STEMI, this is a challenging ECG to most. Pendell Meyers , Aaron E. I suspect most blog readers did not struggle with this one. Baker , Shifa R.
A 12-lead was recorded, showing "STEMI," but is unavailable. Moreover, if you know that catastrophic intracranial hemorrhage can result in an ECG that mimics STEMI, then you know that this patient probably has a severe intracranial hemorrhage. She was BVM ventilated and suctioned. Shortly thereafter, pulses were lost.
Whether your program is primarily 9-1-1, interfacility transport (IFT), or a combination of both, the likelihood of being responsible for the safe and expeditious transport of a STEMI patient is high for anyone in the out-of-hospital care setting. Here are my top 5 recommendations to add to your STEMI bundle of care.
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