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There is LBBB with concordant ST elevation in II and aVF (inferior STEMI) and V6 (lateral STEMI); also concordant ST depression in V2 and V3 (Posterior STEMI). The physician (one of our fine EM residents) caring for the patient did an immediate bedside ultrasound. He complained of chest pain. This ECG was recorded.
Primary percutaneous coronary intervention (PPCI) remains the gold-standard treatment for ST-elevation myocardial infarction (STEMI). We present the case of a man in his 50s, admitted with cardiac arrest secondary to inferolateral STEMI.
This is all suggestive of posterior STEMI, but not definitely diagnostic. mm in only one posterior lead is highly sensitive and specific for posterior STEMI). I performed a bedside cardiac ultrasound and the posterior wall appeared to be contracting and shortening normally. The ECG normalized overnight. Maximum troponin was 2.1
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.
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. At first glance, it seems the patient is having a STEMI. ACS and STEMI generally do not cause tachycardia unless there is cardiogenic shock.
We did a bedside cardiac ultrasound. This is as clear a STEMI as you can get. So this is classic inferoposterior STEMI on the ECG but is NOT acute coronary syndrome! The ECG and ultrasound could not have been differentiated from acute plaque rupture with occlusion of the RCA. 3 points gets you an MI by Sgarbossa.
This is a 45 yo male who had an inferior STEMI 6 months prior, was found to have severe LAD and left main disease, and was supposed to be set up for CABG a few weeks later, but did not follow up. But it could be anterior STEMI. 40% of anterior STEMI has upward concavity in all of leads V2-V6. is likely anterior STEMI).
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.
A male in his 40's who had been discharged 6 hours prior after stenting of an inferoposterior STEMI had sudden severe SOB at home 2 hours prior to calling 911. He had diffuse crackles on exam and B-lines on chest ultrasound, and chest x-ray also confirmed pulmonary edema. Is this acute STEMI? Is this an acute STEMI? -- Unlikely!
The following ECG was recorded: There is an obvious acute inferior STEMI. Whenever there is inferior STEMI, one should think about Right Ventricular STEMI (RVMI). As 85% of inferior STEMI are due to RCA occlusion [the rest due to occlusion of a "dominant" circumflex (i.e., and STE in lead III > STE in lead II.
The conventional machine algorithm interpreted this ECG as STEMI. Answer : Bedside ultrasound! Smith : RV infarct may also have this appearance on ultrasound. So hypoxia without B lines on lung ultrasound strongly weights toward PE. So hypoxia without B lines on lung ultrasound strongly weights toward PE.
4,5] We have now formally studied this question: Emergency department Code STEMI patients with initial electrocardiogram labeled ‘normal’ by computer interpretation: a 7-year retrospective review.[6] have published a number of warnings about the previous reassuring studies.[4,5]
Bedside ultrasound showed no effusion and moderately decreased LV function, with B-lines of pulmonary edema. 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 Learning Points: 1.
This ECG is highly concerning for LAD occlusion despite it not showing a STEMI criteria. You can find the variables used to calculate the value on MD calc here: [link] Utilizing Dr. Smith’s Subtle Anterior STEMI Calculator (4-Variable), the value is greater than 18.2 which is concerning for LAD occlusion.
The cardiologist recognized that there were EKG changes, but did not take the patient for emergent catheterization because the EKG was “not meeting criteria for STEMI”. Troponin was elevated and no “STEMI” was seen on the EKG, so if it is acute MI, then “NSTEMI” is the diagnosis (however flawed), not a pathology on the differential.
She knows the baseline is normal, and she knows the STEMI(-) OMI one is diagnostic of OMI, with the highest possible confidence. Here is the EM decision making: "The patient's EKG revealed some repolarization abnormalities but no clear signs of a STEMI. Gallbladder ultrasound was negative for stones. Chest x-ray was normal.
The computer read Anterior STEMI along with RBBB. I would activate the cath lab based on this and the clinical presentation, but I do NOT see any evidence of anterior STEMI The patient arrived in the ED and had this ECG: The T-waves are now less hyperacute, but ST Elevation remains. Here is his prehospital ECG: What do you think?
The problem is difficult to study because angiographic visualization of arteries is not perfect, and not all angiograms employ intravascular ultrasound (IVUS) to assess for unseen plaque or for plaque whose rupture and ulceration cannot be seen on angiogram. Thus, intracoronary imaging modalities are crucial in this setting. From Gue at al.
This case was posted on the [link] ultrasound site, of which this ECG blog is a part. I refer you to the video case presentation by one of my colleagues, Dr. Rob Reardon (who has, by the way, a fantastic collection of ED ultrasound cases). In this case, the ECG never mimicked a STEMI.
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. Vitals were normal except for oxygen saturation of 94%. Vitals were normal.
Here is his ED ECG at triage: Obvious high lateral OMI that does not quite meet STEMI criteria. Bedside cardiac ultrasound with no obvious wall motion abnormalities. . — He had a previous ECG on file: Proving the findings are new The cath lab was activated. He was given aspirin and sublingual nitro and the pain resolved.
A bedside cardiac ultrasound was recorded: Here is a still image of the echo: The red arrows outline the right ventricle and the yellow arrows outline the left ventricle chamber. Although most cardiac arrest from MI is due to ventricular fibrillation, some is due to high grade AV block, and so this could indeed be due to large acute STEMI.
This is all but diagnostic of STEMI, probably due to wraparound LAD The cath lab was activated. This was diagnosed by IVUS (intravascular ultrasound) as a ruptured plaque. A 40-something male presented with dyspnea and left arm numbness, and perhaps some chest tightness, for 1 1/2 hours. Values: STE60V3 = 2.0, There was good flow.
He reports that this chest pain feels different than prior chest pain when he had his STEMI/OMI, but is unable to further describe chest pain. Arrival at time 0 ECG 7 min Roomed in hallway at 17 min Moved to room with monitor at 37 min The patient was seen briefly by the physician, who then went to get an ultrasound machine.
This was sent by a recent ultrasound fellow, asking for my ECG diagnosis. However, there are morphologies of Takotsubo that cannot be distinguished from STEMI. Takotsubo This looks like and infero-posterior STEMI, but the QT is bizarrely long. There is ST elevation in I, II, III, aVF, V2, V3, V4, V5, and V6.
Bedside ultrasound with no apparent wall motion abnormalities, no pericardial effusion, no right heart strain. 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). Labs ordered but not yet drawn.
This meets "STEMI criteria" However, there is very high voltage, with a very deep S-wave in V2 and tall R-wave in V4. The morphology is not right for STEMI. My interpretation: LVH with secondary ST-T abnormalities, exaggerated by stress, not a STEMI. This is very good evidence that the ST elevation is not due to STEMI.
The receiving emergency physician consulted with interventional cardiology who stated there was no STEMI. However the patient continued to have chest pain and bedside ultrasound showed hypokinesis of the septum with significantly reduced LVEF. Is there STEMI? The patient continued having chest pain. What is the rhythm?
A bedside ultrasound was done, with dozens of clips, and was even done with Speckle Tracking. Because we are hypnotized the STEMI paradigm. "If If there is no STEMI, there is no emergent problem and the patient can wait." It was not a STEMI) 1. To me, this looks like pulmonary edema. Here are a few clips.
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." Cardiac Ultrasound may be a surprisingly easy way to help make the diagnosis Answer: pulmonary embolism. Now another, with ultrasound. What is the Diagnosis? This is a quiz.
There is an obvious inferior posterior STEMI(+) OMI. Case continued A bedside ultrasound showed diminished LV EF and of course bradycardia. Results Of 149 patients with inferior STEMI , 43 (29%) had RVMI and 106 (71%) did not. What is the atrial activity? Is it sinus arrest with junctional escape? How would one tell?
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?
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. This ECG was recorded prehospital, and the computer read STEMI, so the medics activated the cath lab: What do you think? The ECG is consistent with high lateral STEMI. Called 911.
The ECG shows obvious STEMI(+) OMI due to probable proximal LAD occlusion. Another approach is sympathetic chain (stellate ganglion) blockade if you have the skills to do it: it requires some expertise and ultrasound guidance. The pain was 10/10 in intensity radiating bilaterally to the shoulders and also to the left arm and neck.
This case was provided by Spencer Schwartz, an outstanding paramedic at Hennepin EMS who is on Hennepin EMS's specialized "P3" team, a team that receives extra training in advanced procedures such as RSI, thoracostomy, vasopressors, and prehospital ultrasound. Takotsubo is a sudden event, not one with crescendo angina.
Could this be Septal STEMI (STE in V1 and aVR, with reciprocal ST depression in V4-V6?), In Septal STEMI , transmural ischemia of the septum is recorded by the overlying lead V1 as ST Elevation. Lead III is also on the right and might manifest ST Elevation in Septal STEMI. with ADDED STE in III?
EMS recorded these ECGs: Time 0: In V2-V4, there is ST elevation that does not meet STEMI "criteria," of 1.5 Here are a couple shots with strain, or "speckle tracking" on ED Echo: To, me these look like anterior wall motion abnormality, but I showed them to one of our ultrasound fellows who is very interested in this. She called 911.
Prehospital Conventional algorithm interpretation: ANTERIOR INFARCT, STEMI Transformed ECG by PM Cardio: PM Cardio AI Bot interpretation: OMI with High Confidence What do you think? On arrival, lung ultrasound confirmed pulmonary edema (B lines). This is proximal LAD Occlusion until proven otherwise.
After rethinking the case, he remained concerned about ACS and subsequently performed a point-of-care ultrasound in order to evaluate for regional wall motion abnormality. In equivocal cases, point-of-care ultrasound may be the difference between taking the patient to the lab or not. 1] Wereski, R., Chapman, A. Gray, A., &
A bedside ultrasound revealed a possible anterior wall motion abnormality. They may be the only remaining clue to a reperfused LAD occlusion. Today the discomfort is associated with multiple episodes of vomiting and it is unremittant. The following EKG was obtained and hyperkalemia was diagnosed. The K returned at 2.9
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. These ultrasounds confirm LAD occlusion. How do I know?
This is a troponin I level that is almost exclusively seen in STEMI. So this is either a case of MINOCA, or a case of Type II STEMI. If the arrest had another etiology (such as old scar), and the ST elevation is due to severe shock, then it is a type II STEMI. I believe the latter (type II STEMI) is most likely.
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?
Given her risk factors (HTN, HLD, ESRD from diabetes) I decided to obtain a broad cardiac workup for the patient: serial ECGs, labs, serial troponins, CXR and bedside cardiac ultrasound. Ultrasounds can be very helpful in guiding your diagnostic pathway: location of WMA on US led to obtaining posterior leads.
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