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This EKG is diagnostic of transmural ischemia of the inferior wall. If it is angina, lowering the BP with IV Nitroglycerine may completely alleviate the pain and the (unseen) ECG ischemia. Transmural ischemia (as seen with the OMI findings on ECG) is not very common with demand ischemia, but is possible. Smith SW.
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. What should be done? Should the cath lab be activated?
1.196 x STE60 in V3 in mm) + (0.059 x computerized QTc) - (0.326 x RA in V4 in mm) Third, one can do an immediate cardiac ultrasound. A bedside ultrasound was done by an emergency physician and simultaneously read by a cardiologist. greater than 23.4 is likely anterior STEMI). LV aneurysm is very different for inferior vs. anterior MI.
The patient was extubated on Day-3 of the hospital stay. The patient improved, and on Day-11 of the hospital stay — he was off inotropes and on a small dose of a ß-blocker. There is no definite evidence of acute ischemia. (ie, Some residual ischemia in the infarct border might still be present.
The differential is: Posterolateral OMI or subendocardial ischemia The distinction between posterior OMI and subendocardial ischemia can be important and sometimes difficult. Bedside ultrasound is another very important piece. Ischemic ST depression includes posterior OMI and subendocardial ischemia.
In terms of ischemia, there is both a signal of subendocardial ischemia (STD max in V5-V6 with reciprocal STE in aVR) AND a signal of transmural infarction of the inferior wall with Q wave and STE in lead III with reciprocal STD in I and aVL. He spent almost 2 months in the hospital, and reportedly made a full neurologic recovery.
His response: “subendocardial ischemia. Smith : It should be noted that, in subendocardial ischemia, in contrast to OMI, absence of wall motion abnormality is common. With the history of Afib, CTA abdomen was ordered to r/o mesenteric ischemia vs ischemic colitis vs small bowel obstruction. Anything more on history?
This suggests further severe ischemia. 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. And yet the arteries remain open.
Similarly, STEMI guidelines call for urgent angiography for refractory ischemia or electrical/hemodynamic instability, regardless of ECG findings. So there is now high pre-test probability + refractory ischemia + Modified Sgarbossa + dynamic ECG changes. The patient still had chest pain and a third ECG was performed. Learning points 1.
My opinion was that it was not a cath lab case, but I did suggest they do a bedside ultrasound to look for an anterior wall motion abnormality. I had not seen the cardiac ultrasounds at this time. The patient was given aspirin and heparin and admitted to the hospital. I did not have more information at the time.
Down-up T-waves in inferior leads are almost always reciprocal to ischemia in the territory underlying aVL. This is not normal and is a tip off that there is posterior ischemia accompanying the ischemia in aVL. Data from stress testing proves that the ST depression of ischemia does not localize.
He had been seen several weeks ago at an outside hospital for a similar issue and had been discharged home, presumably after unremarkable workup. This proves that the first one was, surprisingly, due to ischemia!! He was ultimately discharged after a brief, uncomplicated hospital course. Peak troponin level unknown.
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. These findings are diagnostic of an apical OMI as a result of LAD Occlusion.
A bedside cardiac ultrasound was performed with a parasternal long axis view demonstrated below: There is a large pericardial effusion with collapse of the right ventricle during systole. She was discharged after a short hospitalization with oncology and cardiology follow-up. This patient is only pseudo-stable.
Dr. Nossen performed a bedside ultrasound which was interpreted as normal. Learning Points: Ectopic atrial rhythm can produce atrial repolarization findings that can be confused for acute ischemia, STEMI, or OMI. The 1st Clue in today's case that cardiac catheterization was probably not needed — is in the History.
Bedside ultrasound showed no effusion and moderately decreased LV function, with B-lines of pulmonary edema. If there is polymorphic VT with a long QT on the baseline ECG, then generally we call that Torsades, but Non-Torsades Polymorphic VT can result from ischemia alone. He was managed medically with Clopidogrel. mg/dL [1.03 0.16
A bedside cardiac ultrasound was normal, with no effusion. 3 studied 416 patients hospitalized with COVID in China, of whom 82 had an initial cTn(I) above the upper reference limit. Association of Cardiac Injury With Mortality in Hospitalized Patients With COVID-19 in Wuhan, China. 3–8 Shi et al. Available from: [link] 3.
Ischemic ST-Segment Depression Maximal in V1-V4 (Versus V5-V6) of Any Amplitude Is Specific for Occlusion Myocardial Infarction (Versus Nonocclusive Ischemia). The patient was started on dual antiplatelet therapy and discharged from the hospital on day 3 without further event. J Am Heart Assoc. 2021 Dec 7;10(23):e022866. 121.022866.
RCA ischemia often results in sinus bradycardia from vagal reflex or ischemia of the sinus node. They did not have an ultrasound on the ambulance (some local crews are starting to utilize POC limited US in our service areas). The patient never arrested during his time at the hospital and his prognosis is good.
He was then transferred to quaternary care childrens hospital. Beware a negative Bedside ultrasound. No apical thrombus noted using Definity contrast. Coxsackie serologies negative. Covid PCR negative. UDS positive for marijuana only. There, troponins were trended up to 100,000 ng/L (still unknown if troponin I or T). Pericarditis?
Case 4 Transient STEMI, serial ECGs prehospital to hospital, all troponins negative (less than 0.04 To me, this makes the ECG nearly diagnostic of ischemia, though if it is LAD occlusion, there should be ST depression in III and aVL, so it is a bit confusing. 100% LAD occlusion. consistent with LAD occlusion) It was not diagnosed.
We computed a Vascular Disease (VasD) score, integrating the presence of carotid plaque (CP) on carotid ultrasound, known coronary artery disease (CAD), and myocardial ischemia (MyI). Subsequently, patients were followed for 5.5 Survival curves depicted a rising risk of the outcome corresponding to increasing VasD scores (Figure 1).Conclusions:The
Check : [vitals, SOB, Chest Pain, Ultrasound] If the patient has Abdominal Pain, Chest Pain, Dyspnea or Hypoxemia, Headache, Hypotension , then these should be considered the primary chief complaint (not syncope). Evidence of acute ischemia (may be subtle) vii. Aortic Dissection, Valvular (especially Aortic Stenosis), Tamponade.
There is no evidence of infarction or ischemia. A bedside POC cardiac ultrasound was done: Findings: Decreased left ventricular systolic function. The patient was given furosemide and admitted to the hospital. There are nonspecific ST-T abnormalities. Troponin I was 0.054 ng/mL NT-ProBNP was 8316 (0-900 pg/mL). "
These ECGs were texted to me by one of our previous ultrasound fellows, Will Smoot An elderly male arrived via EMS for acute substernal chest pain with radiation to left shoulder and arm that awakened him from sleep at 0030. He took two full strength aspirin prior to EMS arrival. The pain was relieved by one prehospital NTG spray.
I suspect pulmonary edema, but we are not given information on presence of B-lines on bedside ultrasound, or CXR findings. Cardiology services were consulted at a PCI capable hospital. The patient was started on heparin for possible NSTEMI vs demand ischemia. Smith : these ECGs do NOT show subendocardial ischemia.
Case continued A bedside cardiac ultrasound revealed grossly preserved left ventricular function, no appreciable wall motion abnormality, pericardial effusion, or obvious valvular abnormality. A good size infarct that no longer has active ischemia will have continually rising troponins due to the damage that was done hours ago.
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