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Are Some Cardiologists Really Limited by Strict Adherence to STEMI millimeter criteria? This is the response he got: Interventionist: "No STEMI, no cath. After stabilizing the patient and recording more ECGs, he tried again: Interventionalist: "It isn't a STEMI." It is a STEMI equivalent. We don't know how many though.
Cardiac arrest #3: ST depression, Is it STEMI? For clarity in Figure-1 — I've reproduced today's ECG — obtained following successful resuscitation of out-of-hospital cardiac arrest. Description of today's ECG findings ( Sinus tachycardia with diffuse ST depression and ST elevation in aVR ) — is diagnostic of DSI.
Prompt cath is therefore advised if the post-ROSC shows an acute STEMI. The rhythm is regular — at a rate just over 100/minute = sinus tachycardia ( ie, the R-R interval is just under 3 large boxes in duration ). Continuing with assessment of ECG #1 in Figure-2: The rhythm is sinus tachycardia at ~110/minute.
She presented to an outside hospital after several days of malaise and feeling unwell. Sinus tachycardia has many potential causes. This is especially true for the elderly patient with sinus tachycardia. What is the cause of the sudden tachycardia? At the time of admission, her vital signs were normal.
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. The patient had a protracted hospitalization and did not survive.
Let me tell you about her hospitalization, discharged 1 day prior, but it was at another hospital (I wish I had the ECG from that hospitalization): The patient is 40 years old and presented to another hospital with chest pain and SOB. She was diagnosed with a Non-STEMI and kept overnight for a next day angiogram.
The patient was promptly admitted to the hospital for further evaluation. While the initial impression might not immediately suggest ventricular tachycardia (VT), a closer examination raises suspicion. An initial electrocardiogram (ECG) is provided below. What do you think? What is the rhythm? The rate is 132 bpm. What is the rhythm?
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. The two cases were considered: Patient 1 was recognized by the ED provider and the cardiologist as having resolved “STEMI”. Patient 1 remained in the hospital overnight.
His friend was able to get him into the truck and drive him to a nearby community hospital (non-PCI center). Is this inferor STEMI? Tachycardia and ST Elevation. Atrial Flutter with Inferior STEMI? The EM provider asked if the cardiologist thought it was a "STEMI." Long-term outcome is unknown.
He was admitted to the hospital for evaluation of these symptoms — but no ECG was done at that time. At 2111, the troponin I peaked at 12.252 ng/mL (this is in the range of STEMI patients, quite high). The conventional computer algorithm called “ sinus tachycardia, otherwise normal EKG ”. The proximal LAD is now widely patent.
He was treated for infection and DKA and admission to hospital was planned. This is ischemic ST depression, and could be due to increasing tachycardia, with a heart rate over 130, but that is unlikely given that the patient is now complaining of crushing chest pain and that there was tachycardia all along.
Despite active CP — cath lab activation was deferred and this patient was transported to a local hospital without PCI capability. It definitely does not fulfill STEMI criteria, and I would argue that it would not lead to cath lab activation in most centers. NOTE #1: Sinus tachycardia is not usually seen in an uncomplicated acute MI.
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. aVR ST segment elevation: acute STEMI or not? aVR ST Segment Elevation: Acute STEMI or Not?
The "criteria" for posterior STEMI are 0.5 Is it STEMI or NonSTEMI? The patient had no hypertension, no tachycardia, a normal hemoglobin, no drug use, no hypotension/shock, no murmur of aortic stenosis. The troponin I returned at 4.1 ng/mL (ULN = 0.030 ng/mL) , diagnostic of myocardial injury. mm STE in one lead.
A previously healthy 53 yo woman was transferred to a receiving hospital in cardiogenic shock. Here was the ECG: There is sinus tachycardia. So Shark Fin really is just a dramatic representation of STEMI, and can be in any coronary distribution. So this is STEMI, right? This was sent by a reader. and K was normal.
The shortened PR-interval, specifically, proved to be quite beguiling as it swept crews down a differential diagnosis of intermittent accessory pathway syndrome – insomuch as a “syndrome” of recurrent tachycardia to account for the patient’s symptoms. To which the lead paramedic replied, “Not cardiac; his symptoms are atypical. Is this OMI?
Is it ventricular tachycardia (VT) due to hyperK or is it a supraventricular rhythm with hyperK? Hospital admission had been recommended, but she left that ED against medical advice. to greatly decrease risk (although in STEMI, the optimal level is about 4.0-4.5 There is some ST depression and peaked T-waves.
His initial cTnI at the receiving hospital was 27 ng/mL, and no further troponins were measured thereafter. Unfortunately there is no echocardiogram accessible because the patient checked himself out of the hospital in order to get back to his home state before it could be completed. To our knowledge, the patient did well.
They informed me that she had just been hospitalized 10 days ago for "some fluid around the heart" and was discharged after one day without incident. Ultimately, she spent several days in the hospital and no further fluid collected. She was diagnosed with pericarditis and spent one day in the hospital without events.
Clinical Course The paramedic activated a “Code STEMI” alert and transported the patient nearly 50 miles to the closest tertiary medical center. Author continued : STE in aVR is often due to left main coronary artery obstruction (OR 4.72), and is associated with in-hospital cardiovascular mortality (OR 5.58). What do you see?
T-wave inversions and dynamic ST elevation Tachycardia, hyperthyroid, and ST elevation. Anterior STEMI? Two cases of ST Elevation with Terminal T-wave Inversion - do either, neither, or both need reperfusion? What is it? 2 Cases of Resolved Chest Pain with Dynamic Terminal T-wave Inversion Is it Wellens' Syndrome?
After admission to the hospital, the patient was discharged from the hospital without any investigation of his acute MI. In such cases, it is common for tachycardia to exaggerate the ST Elevation And, in fact, there was no new acute MI at this visit - troponins did not rise again. See this case: Should Troponin be a Vital Sign?
Admitted to the hospital service for further evaluation and management." Diagnosis: Acute non-ST segment elevation MI (Non-STEMI, or NSTEMI) Second troponin returned at around 0200: 15,894 ng/L 0245 (unclear if ongoing pain or not) Inferoposterior (and lateral V5-6) reperfusion findings. There is sinus tachycardia at 100-105/minute.
Here is his ED ECG: There is obvious infero-posterior STEMI. What are you worried about in addition to his STEMI? Comments: STEMI with hypokalemia, especially with a long QT, puts the patient at very high risk of Torsades or Ventricular fibrillation (see many references, with abstracts, below). There is atrial fibrillation.
ECG is consistent with severe hypokalemia and/or hypomagnesemia causing prolonged QT (QU) at high risk of Torsades (which is polymorphic ventricular tachycardia in the setting of a long QT interval). The patient was admitted to the ICU for close monitoring and electrolyte repletion and had an uneventful hospital course. Is it STEMI?
The ECG shows obvious STEMI(+) OMI due to probable proximal LAD occlusion. The patient was extubated on Day-3 of the hospital stay. The patient improved, and on Day-11 of the hospital stay — he was off inotropes and on a small dose of a ß-blocker. The below ECG was recorded.
There is sinus tachycardia (do not be fooled into thinking this is VT or another wide complex tachycardia!) Code STEMI was activated. A man in his 80s with chest pain What, besides large anterior STEMI, is so ominous about this ECG? in-hospital mortality was 18.8% Protocols can be overridden by Physician Judgment.
3 studied 416 patients hospitalized with COVID in China, of whom 82 had an initial cTn(I) above the upper reference limit. In a series of 18 patients with COVID and ST elevation, 8 were diagnosed with STEMI, 6 of whom had an angiogram and it showed obstructive coronary disease. 3–8 Shi et al. Clin Chem [Internet] 2017;63(1):101–7.
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." Given his exertional chest pain and elevated troponin, the patient was admitted to the hospital for "NSTEMI" with a plan for left heart catheterization the next day. and tachycardia, 1.8.
There is an obvious inferior STEMI, but what else? Besides the obvious inferior STEMI, there is across the precordial leads also, especially in V1. This STE is diagnostic of Right Ventricular STEMI (RV MI). In fact, the STE is widespread, mimicking an anterior STEMI. EKG is pictured below: What do you think?
Other than tachycardia, Other than slight tachycardia, vitals were within normal limits (including oxygen saturation). The provider contacted cardiology to discuss the case, but cardiology "didn't think it was a STEMI, didn't think he needed emergent cath." The whole paradigm is literally called "STEMI" vs. "NSTEMI."
When total LM occlusion does present with STE in aVR, there is ALWAYS ST Elevation elsewhere which makes STEMI obvious; in other words, STE is never limited to only aVR but instead it is part of a massive and usually obvious STEMI. All are, however, clearly massive STEMI. This is her ECG: An obvious STEMI, but which artery?
He spent almost 2 months in the hospital, and reportedly made a full neurologic recovery. This patient arrested shortly after hospital arrival. His course remained complicated — but amazingly, he was discharged from the hospital some 2 months later with intact neurologic status! He was prescribed apixaban.
The attending crews were concerned for SVT with corresponding ischemic hyperacute T waves (HATW) and subsequently activated STEMI pre-hospital. 2] But there is also Sinus Tachycardia! No calcium was administered during pre-hospital transport. A finger-stick glucose resulted 551 mg/dL, and the following ECG was recorded.
Despite the clinical context, Cardiology was consulted due to concerns for a "STEMI". After initiating treatment for hyperkalemia, repeat ECG showed resolution of Brugada pattern: The ECG shows sinus tachycardia. A Very Wide Complex Tachycardia. From Ken Grauer ( See below ) — with this Figure adapted from LITFL.
The status of the patients chest pain at this time is unknown : EKG 1, 1300: There is sinus tachycardia and artifact of low and high frequency. However, there is also significant tachycardia , with heart rate of 116, and known hypoxia. Supply-demand mismatch can cause ST Elevation (Type 2 STEMI). An EKG was immediately recorded.
His first EKG is shown below, with a lead II rhythm strip: EKG 1, 1645 A provisder who is looking for STEMI would not see much in this EKG. It is possible that the T waves in this EKG are of an intermediate morphology between full-blown STEMI and inferior reperfusion. Cardiology was consulted at a PCI-capable hospital.
Ventricular tachycardia?) Why is a patient allowed to present in the hyperacute phase of LAD OMI and complete his infarct in the hospital under physician care? Learning points: 40% of LAD OMI with TIMI-0 flow do NOT meet STEMI criteria (manuscript under consideration at Eur Ht. What do you think? Proximal LAD."
This ECG was recorded: It is difficult to appreciate P-waves, but I believe this is sinus tachycardia. It is correct that he did not have chest pain, but we must remember that fully 1/3 of full blown STEMI do not present with chest pain. This is extremely elevated for a type 2 MI and totally consistent with STEMI.
However, due to the nature of the symptoms, the patient was treated for ACS and admitted to the hospital. Smith comment: Approximately 33% of cases that everyone would call STEMI reperfuse spontaneously (TIMI-1, 2, 3 flow) before they undergo emergent angiogram (usually under 90 minute door to balloon time) 20% have TIMI-3 flow.
The paramedics diagnosis was "Possible Anterolateral STEMI." More proof that a huge STEMI may have normal or near normal initial troponin. A retrospective 'target trial emulation' comparing amiodarone and lidocaine for adult out-of-hospital cardiac arrest resuscitation. The final angiographic result is very good.
Vitals were reported as within normal limits except for tachycardia. Side note: I think the rhythm is probably sinus tachycardia, but I can't easily point out the sinus P waves. ( Without the RBBB, I think most everyone would call this "STEMI." She survived the hospitalization, but long term outcome is not available.
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