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
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? He had no chest pain.
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. Two stents were placed.
A man in his mid 60s with history of CAD and stents experienced sudden onset epigastric abdominal pain radiating up into his chest at home, waking him from sleep. She knows the baseline is normal, and she knows the STEMI(-) OMI one is diagnostic of OMI, with the highest possible confidence. It is stented with good angiographic result.
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.
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 The culprit mid LAD lesion was stented.
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? This was stented. to greatly decrease risk (although in STEMI, the optimal level is about 4.0-4.5
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.
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 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. It was stented. 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,
On intravascular ultrasound (IVUS), the mid RCA plaque was described as "cratered, inflamed, and bulky," and the OM plaque was described as "bulky with evidence of inflammation and probably ulceration." On the combined basis of angiography and IVUS, this patient received stents to his mid RCA, proximal PDA, and OM.
A middle-aged male with h/o CAD and stents presented with typical chest pressure. 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. So there is pathologic ST elevation here, consistent with anterolateral STEMI. Called 911.
There is an obvious inferior posterior STEMI(+) OMI. Case continued A bedside ultrasound showed diminished LV EF and of course bradycardia. Angiogram: Culprit Lesion (s): Thrombotic occlusion of the proximal RCA -- stented. Results Of 149 patients with inferior STEMI , 43 (29%) had RVMI and 106 (71%) did not.
He underwent coronary stenting (uncertain which artery). An emergency cardiac ultrasound could be very useful. He underwent immediate CPR, was found to be in ventricular fibrillation, and was successfully resuscitated. I do not have the post-resuscitation ECG. Could this have been avoided?
A bedside ultrasound revealed a possible anterior wall motion abnormality. There was an LAD occlusion that was opened and stented. They may be the only remaining clue to a reperfused LAD occlusion. The patient was treated with Calcium, Insulin, D50, and bicarbonate, with no change in the ECG. The K returned at 2.9
The patient was brought to the ED as a possible Code STEMI and was seen directly by cardiology. Similarly, STEMI guidelines call for urgent angiography for refractory ischemia or electrical/hemodynamic instability, regardless of ECG findings. So the RCA was stented. Vitals were HR 58 BP 167/70 R20 sat 96%.
Two thirds of MINOCA cases are due to atherosclerotic causes One way to prove the diagnosis in this case would have been with intravascular imaging such as optical coherence tomography (OCT) or intravascular ultrasound (IVUS). Fortunately, that is exactly what happened. The patient did well afterward without any recurrence of symptoms.
This was a point of care ultrasound, not a bubble contrast echo. One would not expect wall motion to recover so quickly after stenting, so this is good evidence that the POCUS echo was indeed accurate. What do you think the echocardiogram shows? First trop I returns at 1.5. Is this OMI?
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. It was stented.
It was opened and stented. Important Learning Point: "STEMI" is defined by millimeter criteria (1 mm in limb leads), which this does not meet. Therefore it is not a STEMI. But what we truly care about is coronary occlusion, for which STEMI is just a surrogate that is only about 75% sensitive for occlusion. RCA: dominant.
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. He was successfully treated with one drug eluting stent. A second troponin had been drawn 3 hours after arrival and was again less than 0.30ng/mL. 1] Wereski, R.,
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. He was successfully stented.
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)? Appropriately, the physicians repeated the ECG 20 minutes later and it was diagnostic of anterior STEMI. QTc is the computer measurement. 100% LAD occlusion.
EMS recorded these prehospital ECGs: Time 0: In V2-V4, there is ST elevation that does not meet STEMI "criteria," of 1.5 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 was having a transient STEMI, briefly. It was stented.
Immediate and early percutaneous coronary intervention in very high-risk and high-risk Non-STEMI patients. Smith comment: Point of Care ultrasound is not adequate to rule out wall motion abnormality; moreover, diffuse subendocardial ischemia often has no wall motion abnormality because the epicardium is still contracting. mg/dL, K 3.5
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. It was thought to be an in stent restenosis and thrombosis from a DES placed in the same region 6 months prior. There was initially TIMI 0 flow.
Case continued A bedside cardiac ultrasound revealed grossly preserved left ventricular function, no appreciable wall motion abnormality, pericardial effusion, or obvious valvular abnormality. The terminal part of the T-wave is inverted in lead III, and reciprocally terminally upright in lead aVL.
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