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The Case A 71-year-old male with a history of chronic obstructive pulmonary disease, hyperlipidemia, and peptic ulcer disease presents to the emergencydepartment with substernal chest pain radiating down the right arm and dyspnea that began acutely while “running” up the stairs from the subway.
Traditionally, emergency providers looked for signs of ST-segment elevation myocardial infarction (STEMI) to indicate the need for intervention. Emergency physicians have recognized for some time that there are many occlusions of the coronary arteries that do not present with classic STEMI criteria on the ECG.
The Case A 71-year-old male with a history of chronic obstructive pulmonary disease, hyperlipidemia, and peptic ulcer disease presents to the emergencydepartment with substernal chest pain radiating down the right arm and dyspnea that began acutely while “running” up the stairs from the subway.
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]
Written by Jesse McLaren A 70 year old with prior MIs and stents to LAD and RCA presented to the emergencydepartment with 2 weeks of increasing exertional chest pain radiating to the left arm, associated with nausea. I sent this to the Queen of Hearts So the ECG is both STEMI negative and has no subtle diagnostic signs of occlusion.
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! Despite serial ECGs being "STEMI negative", the cath lab was activated.
The specific ST/T pattern was not fully appreciated by the attending EMS personnel, yet alarming enough to convince the patient to be seen in the EmergencyDepartment despite his intentions of seeking evaluation on his own accord through his respective family physician. it has been subsequently deemed a STEMI-equivalent.
She arrives in the emergencydepartment (ED) with decreased level of consciousness and shock. Acute coronary syndrome (ACS) is responsible for the majority (60%) of all OHCAs in patients. She has a history of hypertension and non-insulin dependent diabetes mellitus.
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.
If you were working in a busy emergencydepartment, would you like to be interrupted to interpret these ECGs or can these patients safely wait to be seen because of the normal computer interpretation? have published a number of warnings about the previous reassuring studies.[4,5]
, tells us that we physicians do not need to even look at this ECG until the patient is placed in a room because the computer says it is normal: Validity of Computer-interpreted “Normal” and “Otherwise Normal” ECG in EmergencyDepartment Triage Patients I reviewed this article for a different journal and recommended rejection and it was rejected.
The scan also showed “scattered coronary artery plaques”. __ Smith comment 1 : the appropriate management at this point is to lower the blood pressure (lower afterload, which increases myocardial oxygen demand). They too have dense white masses consistent with coronary atherosclerosis. The blue circle shows the LCx. Murakami MM.
Reference: emDOCs – NCSE Journal of Emergency Medicine – Review Case 4: 52-year-0ld male brought in by EMS with “code STEMI” ECG demonstrates ST depressions with rocket like T waves in V2-V4. This document covers high sensitivity troponin, risk disposition pathways, and STEMI equivalents.
According to this data a triage ECG labeled ‘normal’ rules out the possibility of acute coronary occlusion. We also studied 7 years of Code STEMI patients requiring emergent reperfusion, and found that 4% presented with an ECG labeled ‘normal’, often confirmed by the final blinded interpretation.
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.
2: STREAM-2 RCT | Half-Dose Tenecteplase for STEMI Spoon Feed The STREAM-2 trial found half-dose tenecteplase was effective in treating STEMI patients ≥60, though with increased risk of intracranial hemorrhage. Epub 2023 Apr 20. #2:
Written by Bobby Nicholson, MD 67 year old male with history of hypertension and hyperlipidemia presented to the EmergencyDepartment via ambulance with midsternal nonradiating chest pain and dyspnea on exertion. Pain improved to 1/10 after EMS administers 324 mg aspirin and the following EKG is obtained at triage. What do you think?
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. Mimics of ST elevation myocardial infarction (STEMI). Click to enlarge.)
Written by Destiny Folk, MD, Adam Engberg, MD, and Vitaliy Belyshev MD A man in his early 60s with a past medical history of hypertension, type 2 diabetes, obesity, and hyperlipidemia presented to the emergencydepartment for evaluation of chest pain. 4) Lastly, the QRS amplitude in V2 (both the R- and S- waves) are measured.
Written by Bobby Nicholson What do you think of this “STEMI”? A man in his 90s with a history of HTN, CKD, COPD, and OSA presented to the emergencydepartment after being found unresponsive at home. Vital signs were within normal limits on arrival to the EmergencyDepartment. Blood glucose was not low at 162 mg/dL.
This was sent by anonymous The patient is a 55-year-old male who presented to the emergencydepartment after approximately 3 to 4 days of intermittent central boring chest pain initially responsive to nitroglycerin, but is now more constant and not responsive to nitroglycerin. It is unknown when this pain recurred and became constant.
He is transported to the EmergencyDepartment where care is transferred to a nurse. At the hospital a 12-lead ECG is recorded within 10 minutes and read by the attending physician, who activates the “Code STEMI” protocol. Is this a STEMI? So technically it is a STEMI equivalent. The answer is yes!
Many systems now refrain from showing computer "normal" ECGs to the busy emergency physicians at triage because of very poorly conceived articles that say that if the computer algorithm says "normal," the emergency physician should not be bothered. It is clearly missed by the conventional algorithm. No further follow up is available.
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.
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.
Upon arrival to the emergencydepartment, a senior emergency physician looked at the ECG and said "Nothing too exciting." Hospital Course The patient was taken emergently to the cath lab which did not reveal any significant coronary artery disease, but she was noted to have reduced EF consistent with Takotsubo cardiomyopathy.
He presented to the EmergencyDepartment with a blood pressure of 111/66 and a pulse of 117. He was rushed by residents into our critical care room with a diagnosis of STEMI, and they handed me this ECG: There is sinus tachycardia with ST elevation in II, III, and aVF, as well as V4-V6. He had this ECG recorded. The HCO3 was 8.
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.
Written by Colin Jenkins and Nhu-Nguyen Le with edits by Willy Frick and by Smith A 46-year-old male presented to the emergencydepartment with 2 days of heavy substernal chest pain and nausea. The receiving emergency physician consulted with interventional cardiology who stated there was no STEMI. Is there STEMI?
Written by Kaley El-Arab MD, edits by Pendell Meyers and Stephen Smith A 61-year-old male with hypertension and hyperlipidemia presented to the emergencydepartment for chest tightness radiating to the back of his neck that has been intermittent for the past day or two. It is true this ECG does not meet STEMI criteria (there is 1.0
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.
A 56 year old male with a history of diabetes, dyslipidemia, hypertension, and coronary artery disease presented to the emergencydepartment with sudden onset weakness, fatigue, lethargy, and confusion. At 2111, the troponin I peaked at 12.252 ng/mL (this is in the range of STEMI patients, quite high).
20% of cases that everyone would call a STEMI have a competely open artery by the time of angiogram 60-90 minutes later. Angiogram: Severe two-vessel coronary artery disease with possible co-culprits (90% proximal circumflex, 70% mid/distal RCA) in the setting of non-ST elevation myocardial infarction.
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. Could it be acute (vs.
AslangerE A 65-year-old gentleman presented to the emergencydepartment after experiencing two recent ICD shocks in the preceding hours. A recent angiogram report indicated a totally occluded left anterior descending artery (LAD) and right coronary artery (RCA), with 30-40% narrowings in the left circumflex artery (LCx).
A 50 year old presented to the emergencydepartment of a remote rural community (where the nearest cath lab is a plane ride away) with one hour of mild chest pain radiating to the back and jaw, and an ECG labeled ‘normal’ by the computer interpretation. The Need for Immediate Transport?
A 59-year-old male with a past medical history of a repaired ventricular septal defect (VSD), dextrocardia, hypertension, hyperlipidemia, and current smoker presented to the emergencydepartment (ED). Figure 1: EKG for Dextrocardia showing STEMI. The second EKG was concerning for STEMI in the precordial leads (see figure 1).
This page summarises the most current recommendations for the management of acute coronary syndromes with persistent ST-segment elevations (i.e STEMI , ST-segment elevation acute myocardial infarction ). I B Patients transferred to PCI centres can bypass the emergencydepartment to undergo primary PCI without delay.
It was ongoing on arrival in the emergencydepartment. But because there was no new ST elevation, the ECG was signed off as “STEMI negative” and the patient waited to be seen. The emergency physician was called to see the patient 90 minutes later after the troponin I returned at 1100 ng/L. What do you think?
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? Incidence of an acute coronary occlusion.
This was a male in his 50's with a history of hypertension and possible diabetes mellitus who presented to the emergencydepartment with a history of squeezing chest pain, lasting 5 minutes at a time, with several episodes over the past couple of months. New ST elevation diagnostic of STEMI [equation value = 25.3 de Wood et al.
I want all to know that, with the right mind preparation, and the use of the early repol/LAD occlusion formula, extremely subtle coronary occlusion can be detected prospectively, with no other information than the ECG. His ECG was repeated at this point: This shows a well developed anterior STEMI. Ann Emerg Med 1998;31(1):3-11.
Note that they finally have laid to rest the new or presumably new LBBB as a criteria for STEMI. Note that they finally have laid to rest the new or presumably new LBBB as a criteria for STEMI. Also note that they allow ST depression c/w posterior MI to be a STEMI equivalent. Kurkciyan et al.
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