This site uses cookies to improve your experience. To help us insure we adhere to various privacy regulations, please select your country/region of residence. If you do not select a country, we will assume you are from the United States. Select your Cookie Settings or view our Privacy Policy and Terms of Use.
Cookie Settings
Cookies and similar technologies are used on this website for proper function of the website, for tracking performance analytics and for marketing purposes. We and some of our third-party providers may use cookie data for various purposes. Please review the cookie settings below and choose your preference.
Used for the proper function of the website
Used for monitoring website traffic and interactions
Cookie Settings
Cookies and similar technologies are used on this website for proper function of the website, for tracking performance analytics and for marketing purposes. We and some of our third-party providers may use cookie data for various purposes. Please review the cookie settings below and choose your preference.
Strictly Necessary: Used for the proper function of the website
Performance/Analytics: Used for monitoring website traffic and interactions
Primary percutaneous coronary intervention (PPCI) remains the gold-standard treatment for ST-elevation myocardialinfarction (STEMI). We present the case of a man in his 50s, admitted with cardiac arrest secondary to inferolateral STEMI.
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.
An emergency cardiac ultrasound could be very useful. The upright portion of the T-wave in aVF is very large compared to the QRS size. These findings mandate that the patient at least get serial ECGs. If these remain unchanged, then serial troponins.
A bedside ultrasound was done, with dozens of clips, and was even done with Speckle Tracking. Angiogram: "ACS - Non ST Elevation MyocardialInfarction. This is a HUGE myocardialinfarction. Because we are hypnotized the STEMI paradigm. "If It was not a STEMI) 1. To me, this looks like pulmonary edema.
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. MINOCA I do not have the bandwidth here to write a review of MINOCA. Lindahl et al.
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. Am Heart J.
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”. Diagnosis of Type I vs. Type II MyocardialInfarction in Emergency Department patients with Ischemic Symptoms (abstract 102). Murakami MM.
There is an obvious inferior posterior STEMI(+) OMI. Case continued A bedside ultrasound showed diminished LV EF and of course bradycardia. Literature cited In inferior myocardialinfarction, neither ST elevation in lead V1 nor ST depression in lead I are reliable findings for the diagnosis of right ventricular infarction Johanna E.
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. Learning Points: 1.
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?
This is a troponin I level that is almost exclusively seen in STEMI. In this case, profound shock for 1 hour would result in the same degree of infarction. A followup ECG was recorded 2 days later: No definite evidence of infarction. So this is either a case of MINOCA, or a case of Type II STEMI. Troponin I rose to 44.1
Both of these patterns together suggest Aslanger's pattern , recently published in J Electrocardiology: A new electrocardiographic pattern indicating inferior myocardialinfarction. Could this be Septal STEMI (STE in V1 and aVR, with reciprocal ST depression in V4-V6?), These suggest inferior OMI with possible RV involvement.
So there is probability of myocardial injury here (and because it is in the correct clinical setting, then myocardialinfarction.) HsTnI drawn at that time was 9 ng/L (ref. 80%) and definitely too much for hour to hour. From angiography, it is not clear what the culprit is. The ECG changes were inferior, posterior, and lateral.
Smith, MD – Department of Emergency Medicine, Hennepin County Medical Center, Professor, University of Minnesota School of Medicine, Minneapolis, MN ABSTRACT: Background: Patients with type 1 myocardialinfarction with normal left ventricular function that are hemodynamically stable do not usually manifest with sinus tachycardia.
Here is the ED ECG on arrival: Less STE/STD Provider's Clinical Impression: "findings concerning for myocardialinfarction, likely proximal LAD or Left main." This was a point of care ultrasound, not a bubble contrast echo. Cath lab activated Dual antiplatelet therapy and heparin given. NTG drip started. Pain better still.
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.
No pericardial effusion on ultrasound." See our publication: ST depression in lead aVL differentiates inferior ST-elevation myocardialinfarction from pericarditis There is STE in inferior leads, high lateral leads, and V4-V6. Smith and Meyers to diagnose both obvious (STEMI) and subtle OMI. What do you think?
Here is the repeat ECG at 52 minutes after arrival to triage: Obvious posterolateral STEMI Angiographic findings: 1. Regional wall motion abnormality-inferolateral (this is the formal ultrasound location of a posterior wall motion abnormality). After return from CT, the patient's pain was severe again. 2022.08.750 Section 5.2.2,
Electrocardiographic Differentiation of Early Repolarization FromSubtle Anterior ST-Segment Elevation MyocardialInfarction. These kinds of cases were excluded from the study as obvious anterior STEMI. --QTc Case 1 Acute anterior STEMI from LAD occlusion, or Benign Early Repolarization (BER)? 100% LAD occlusion.
A recent study found that SCAD causes almost 20% of STEMI in young women. Often, intravascular ultrasound or intravascular optical coherence tomography is requeried to make the diagnosis. examined SCAD presenting as STEMI (unlike Hassan et al. Type 2 is more difficult to appreciate on angiography than type 1. Lobo et al.
Smith comment: This patient did not have a bedside ultrasound. Had one been done, it would have shown a feature that is apparent on this ultrasound (however, this patient's LV function would not be as good as in this clip): This is recorded with the LV on the right. In fact, bedside ultrasound might even find severe aortic stenosis.
Immediate and early percutaneous coronary intervention in very high-risk and high-risk Non-STEMI patients. Association between opioid analgesia and delays to cardiac catheterization of patients with occlusion MyocardialInfarctions. Unfortunately, they follow their own guidelines only 6% of the time!! Lupu L, et al. mg/dL, K 3.5
Ischemic ST-Segment Depression Maximal in V1-V4 (Versus V5-V6) of Any Amplitude Is Specific for Occlusion MyocardialInfarction (Versus Nonocclusive Ischemia). Recall that air is a poor conductor of electricity and will, therefore, generate smaller amplitudes on posterior leads (hence why STEMI criteria requires only >0.5
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.
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.
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.
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. Do not treat AIVR.
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. First, the name (MyocardialInfarction or Not) is not important. Here is his triage ECG: There is massive STE in V3-V6, and also STE in II, III, aVF.
A bedside cardiac ultrasound was normal, with no effusion. Clin Chem [Internet] 2020;Available from: [link] Smith mini-review: Troponin in Emergency Department COVID patients Cardiac Troponin (cTn) is a nonspecific marker of myocardial injury. 12 All STEMI patients had very high cTn typical of STEMI (cTnT > 1.0
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?
The ECG shows obvious STEMI(+) OMI due to probable proximal LAD occlusion. Troponin T peaked at 38,398 ng/L ( = a very large myocardialinfarction, but not massive-- thanks to the pre-PCI spontaneous reperfusion, and rapid internvention!! ). The below ECG was recorded. Inotropic medication was continued.
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., &
His ED cardiac ultrasound (which is not at all ideal for detecting wall motion abnormalities, and is also very operator dependent for this finding) was significant for depressed global EF. Occlusion MyocardialInfarction (OMI) often does not present with diagnostic ST elevation, or even any STE, especially in dialysis patients.
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?
A middle aged patient who was 3 weeks s/p STEMI came from cardiac rehab where he developed some chest pain, dyspnea and weakness on the treadmill. There is no acute STEMI. This is diagnostic of recent, reperfused STEMI. This is diagnostic of recent, reperfused STEMI. Acute STEMI would have upright T-waves.
She had this ECG recorded: Obvious massive anterior STEMI She was quickly brought to the critical care area and the cath lab was activated. Here is the ECG at 25 minutes: Terrible LAD STEMI (+) OMI So a CT scan was done which of course showed a normal aorta. And almost all of them could be detected by bedside ultrasound.
Nevertheless, the operator performed intravascular ultrasound and saw erupted calcium nodule consistent with plaque erosion. Limitations of registry data: This patient presented with STEMI (-) OMI and developed STEMI the following day. In the world of STEMI, we are incapable of recognizing the first ECG as a false negative.
The paramedics diagnosis was "Possible Anterolateral STEMI." On arrival in the ED, a bedside ultrasound showed poor LV function (as predicted by the Queen of Hearts) with diffuse B-lines. More proof that a huge STEMI may have normal or near normal initial troponin. I don't know what the device algorithm interpretation stated.
We organize all of the trending information in your field so you don't have to. Join thousands of users and stay up to date on the latest articles your peers are reading.
You know about us, now we want to get to know you!
Let's personalize your content
Let's get even more personalized
We recognize your account from another site in our network, please click 'Send Email' below to continue with verifying your account and setting a password.
Let's personalize your content