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Written by Jesse McLaren A previously healthy 50 year-old presented with 24 hours of intermittent exertional chestpain, radiating to the arms and associated with shortness of breath. In a previously healthy patient with new and ongoing chestpain, this is concerning for acute occlusion of the first diagonal artery.
Sent by anonymous, written by Pendell Meyers A man in his 50s with no prior known medical history presented to the Emergency Department with severe intermittent chestpain. He denied any lightheadedness, shortness of breath, vomiting, or abdominal pain. Barely any STE, and thus not meeting STEMI criteria.
Written by Jesse McLaren A 70 year old with prior MIs and stents to LAD and RCA presented to the emergency department with 2 weeks of increasing exertional chestpain 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.
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). Because the patient had no chestpain or shortness of breath, they were initially diagnosed as gastroenteritis. Potassium was normal. Take home 1.
A middle aged male presented at midnight after 14 hours of constant, severe substernal chestpain, radiating to his throat and to bilateral jaws, and associated with diaphoresis. The pain was not positional, pleuritic, or reproducible. The "criteria" for posterior STEMI are 0.5 Is it STEMI or NonSTEMI?
A 70-year-old man calls 911 after experiencing sudden, severe chestpain. The precordial ST-depression pattern on this ECG (and in this clinical setting) should immediately raise suspicion of Posterior STEMI! But if there is none - then you are looking at least at an Isolated Posterior STEMI until proven otherwise.
Submitted and written by Megan Lieb, DO with edits by Bracey, Smith, Meyers, and Grauer A 50-ish year old man with ICD presented to the emergency department with substernal chestpain for 3 hours prior to arrival. At this time he reported ongoing chestpain and was given aspirin and nitroglycerin.
Of course this depends on many factors: 1) duration of occlusion, 2) whether full or near occlusion with zero flow or some flow -- the flow in the artery is the critical factor, measured by "TIMI" flow, 3) presence of collateral circulation and others. Upon questioning patient, he denies having any chestpain or chest tightness of any sort.
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. A mong patients with STEMI, ventricular septal rupture is the most common and free wall rupture is the least common.
He had no previous history of CAD, and presented with very typical waxing and waning chestpain, much worse with exertion but also present at rest and on presentation, though his pain was minimal at the time of the ECG. This is all suggestive of posterior STEMI, but not definitely diagnostic. Blood pressure was 150/80.
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. Circulation 1999;99(15):1972-7.
Despite the absence of significant coronary stenosis on her post-arrest cath — the ECG in Figure-1 is clearly diagnostic of an extensive anterolateral STEMI ( presumably from acute LAD [ L eft A nterior D escending ] coronary artery occlusion). The rhythm in ECG #1 is regular and supraventricular at a rate of ~75/minute.
A middle aged male presented with chestpain. LVH and the diagnosis of STEMI - how should we apply the current guidelines? In LVH, T-wave inversions are usually much more assymetric , like these (Figure 2): Acute Chestpain, but baseline ECG. How about diagnosing anterior STEMI in the setting of LVH?
But, in a patient who presents to the ED for new chestpain — seeing these subtle findings that are localized to leads V2- thru -V4 should at the least make you consider acute posterior OMI ( O cclusion-based MI ) — until you prove otherwise. To EMPHASIZE: These are subtle findings. What do YOU think?
A 70-something female with no previous cardiac history presented with acute chestpain. She awoke from sleep last night around 4:45 AM (3 hours prior to arrival) with pain that originated in her mid back. She stated the pain was achy/crampy. Over the course of the next hour, this pain turned into a pressure in her chest.
Jesse McLaren (@ECGcases), of Emergency Medicine Cases Reviewed by Pendell Meyers and Steve Smith An 85yo with a history of hypertension developed chestpain and collapsed, and had bystander CPR. The patient was brought to the ED as a possible Code STEMI and was seen directly by cardiology. So the RCA was stented.
A middle aged male with no h/o CAD presented with one week of crescendo exertional angina, and had chestpain at the time of the first ECG: Here is the patient's previous ECG: Here is the patient's presenting ED ECG: There is isolated ST depression in precordial leads, deeper in V2 - V4 than in V5 or V6. There is no ST elevation.
Here is his ED ECG at triage: Obvious high lateral OMI that does not quite meet STEMI criteria. He was given aspirin and sublingual nitro and the pain resolved. The history is concerning ( This patient was awakened from sleep by chestpain that persisted for several hours — on a background of intermittent CP in recent weeks ).
This fantastic case and post was written by Jesse McLaren (@ECGcases), edited by Smith Case You’re shown an ECG from a patient in the waiting room with chestpain. Step 1 to missing posterior MI is relying on the STEMI criteria. But it is still STEMI negative. What do you think? A 15 lead ECG was done (below).
By definition, this is a non-STEMI because there is not 1 mm of ST elevation in 2 consecutive leads. However, ST elevation is only an imperfect surrogate for complete acute persistent occlusion of an epicardial coronary artery without collateral circulation. The pain is very nitroglycerine responsive.
This male in his 40's had been having intermittent chestpain for one week. He awoke from sleep with crushing central chestpain and called ems. EMS recorded a 12-lead, then gave 2 sublingual nitros with complete relief of pain. Type B waves are deeper and symmetric.
This was a male in his 50's with a history of hypertension and possible diabetes mellitus who presented to the emergency department with a history of squeezing chestpain, lasting 5 minutes at a time, with several episodes over the past couple of months. Plan was for admission for chestpain workup. Jernberg T, et al.
Later, I found old ECGs: 5 month prior in clinic: V5 and V6 look like OMI 9 months prior in clinic with no chest symptoms: V5 and V6 look like OMI 1 year prior in the ED with chestpain: V5 and V6 sure look like a STEMI For this ECG and chestpain in the ED, the Cath lab activated. There was no OMI.
This patient, who is a mid 60s female with a history of hypertension, hyperlipidemia and GERD, called 911 because of chestpain. A mid 60s woman with history of hypertension, hyperlipidemia, and GERD called 911 for chestpain. It is also NOT the clinical scenario of takotsubo (a week of intermittent chestpain).
Although the patient reported experiencing mild pressure-like chestpain, there was suspicion among clinicians that this might be indicative of an older change. There is some ST-segment elevation in DII, DIII, aVF, V4-6. Due to the observed ST-segment elevation, the medical team expressed immediate concern.
It is equivalent to a transient STEMI. Not much, but studies of STEMI and NonSTEMI show that about 70% of those diagnosed with STEMI have a peak troponin I above 10 ng/mL and that about 70% of those diagnosed with NonSTEMI have a peak troponin I below 10 ng/mL. Circulation. Circulation, 137(19), p.e523. Hayes, S.N.,
Written by Colin Jenkins and Nhu-Nguyen Le with edits by Willy Frick and by Smith A 46-year-old male presented to the emergency department with 2 days of heavy substernal chestpain and nausea. The patient continued having chestpain. Is there STEMI? Circulation Research , 56 (2), 184–194. link] Fesmire, F.
Case A 39-year-old male without prior medical history presents with chestpain that started 2 hours prior to presentation. He says that the pain intensity was 10/10 at home but now about 4/10. Despite the clinical stability and decreasing pain, this patient needs an immediate angiogram. Circulation 2002; 105(4): 539-42.
It was edited by Smith CASE : A 52-year-old male with a past medical history of hypertension and COPD summoned EMS with complaints of chestpain, weakness and nausea. Clinical Course The paramedic activated a “Code STEMI” alert and transported the patient nearly 50 miles to the closest tertiary medical center. Circulation.
Case submitted and written by Dr. Mazen El-Baba and Dr. Emily Austin, with edits from Jesse McLaren A 50 year-old patient presented to the Emergency Department with sudden onset chestpain that began 14-hours ago. This doesn’t meet STEMI criteria so in the current paradigm there’s no urgency to getting an angiogram.
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." See this case: Persistent ChestPain, an Elevated Troponin, and a Normal ECG. Circulation , 130 (25). At midnight.
A male in late middle age with a history of RCA stent 8 years prior complained of chestpain. Here are three more dramatic cases that illustrate RBBB + LAFB Case 1 of cardiac arrest with unrecognized STEMI, died. EMS recorded the following ECG: What do you see?
A late middle-aged man presented with one hour of chestpain. Here is his ED ECG: There is obvious infero-posterior STEMI. What are you worried about in addition to his STEMI? to greatly decrease risk (although in STEMI, the optimal level is about 4.0-4.5 Most recent echo showed EF of 60%. If the patient is at 1.8,
A man in his 60's presented after 4 days of chestpain, with some increase of pain on the day of presentation. Exact pain history was difficult to ascertain. Thus, this is both an anterior and inferior STEMI. How old is this antero-inferior STEMI? Circulation 1993;88(3):896-904. There was some SOB.
A man in his 60's presented after 4 days of chestpain, with some increase of pain on the day of presentation. Exact pain history was difficult to ascertain. Thus, this is BOTH an anterior and inferior STEMI in the setting of RBBB. How old is this antero-inferior STEMI? Circulation 1993;88(3):896-904.
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. N Engl J Med [Internet] 2019;Available from: [link] Should all patients with shockable arrest be taken to angiography regardless of STEMI or No STEMI?
A 65 year old with diabetes presented with a syncopal episode while sitting, associated with weakness but no chestpain or shortness of breath. So they took the patient urgently to cath: 100% occlusion of inferior obtuse marginal branch of the circumflex, with collateral circulation. What do you think?
He denied chestpain or shortness of breath. In the clinical context of weakness and fever, without chestpain or shortness of breath, the likelihood of Brugada pattern is obviously much higher. Circulation, 117, 1890–1893. [3]: See below for PM Cardio digitized version of this. PM Cardio digitized version.
It may be difficult to read STEMI in the setting of RBBB. There is, however, a long QT also, with abnormal T-waves, but this is not STEMI. Case 3 : Male in 30's with chestpain, cough, and fever. This ECG was recorded prehospital, and the computer read STEMI, so the medics activated the cath lab: What do you think?
The patient in today’s case is a previously healthy 40-something male who contacted EMS due to acute onset crushing chestpain. The pain was 10/10 in intensity radiating bilaterally to the shoulders and also to the left arm and neck. The ECG shows obvious STEMI(+) OMI due to probable proximal LAD occlusion.
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?
A middle-aged woman had intermittent angina for 48 hours, then onset of constant, crushing chestpain for 1.5 cm diameter in the apex The presence of thrombus led the clinicians to state that this was a "late presentation STEMI." Circulation 1993; 88:896-904. Circulation 1995; 91:1659-1668. LV Thrombus , 1.5
2) The STE in V1 and V2 has an R'-wave and downsloping ST segments, very atypical for STEMI. Cardiology was consulted and they agreed that the EKG had an atypical morphology for STEMI and did not activate the cath lab. It was from a patient with chestpain: Note the obvious Brugada pattern. Circulation, 117, 1890–1893. [3]:
A 69 year old woman with a history of hypertension presented to the emergency department by EMS for evaluation of chestpain and shortness of breath. She awoke in the morning with sharp chestpain which worsened throughout the morning. As her pain worsened, so did her dyspnea. Also see these posts of Type II STEMI.
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