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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. My Comment , by K EN G RAUER, MD ( 10/24/2018 ): = Important teaching points are made in this post by Dr. Smith. Values: STE60V3 = 2.0, There was good flow.
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?
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.
This was a point of care ultrasound, not a bubble contrast echo. Nevertheless, this ECG pattern of subendocardial ischemia needs to be instantly recognized — so that optimal decision-making based on the clinical scenario can promptly begin ( See the October 31, 2018 post on Dr. Smith’s Blog ). First trop I returns at 1.5. Is this OMI?
Angie Lobo ( @aloboMD ) (For open-access reviews of this literature, see Saw 2016 , Saw 2017 , or Hayes 2018.) 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. A study by Hassan et al.
These kinds of cases were excluded from the study as obvious anterior STEMI. --QTc Am J Cardiol 2018; 122(8):1303-1309. 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.
Exclusion criteria were age less than 18, SBP less than 100 mmHg, echocardiogram with EF less than 50%, STEMI, pregnancy, and trauma. My Comment, by KEN GRAUER, MD ( 6/17/2018 ): = Excellent case with insightful learning points explaining why these serial tracings are not indicative of acute inferior infarction.
Journal of Electrocardiology 2018. However, in almost every case, one should confirm absence of OMI (Occlusion MI) at least by contrast ultrasound. See this case: Pericarditis, or Anterior STEMI? Journal of Emergency Medicine 2006; 31(1):67-77. 40-50% of LAD occlusion have zero reciprocal ST depression. That may be the case.
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. The patient's initial troponin I was 2.0 ng/mL (99% reference level = 0.030 ng/mL. With his ESRD, he does have an elevated baseline troponin at ~0.40
They recorded a prehospital ECG and diagnosed STEMI and activated the cath lab prehospital. ALL TROPS WERE UNDETECTABLE A formal ultrasound was done: Normal estimated left ventricular ejection fraction at rest. When medics arrived, he denied any chest pain, shortness of breath, or palpitations prior to the syncopal episode.
A bedside cardiac ultrasound revealed grossly normal to hyperdynamic systolic function with no obvious areas of wall motion abnormalities. Heart Rhythm 2018. This was recorded about 30 minutes later: Same A previous ECG was obtained and was normal. His lab workup was significant for positive influenza A rapid test and hyponatremia.
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