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Bedside cardiac ultrasound with no obvious wall motion abnormalities. This confirms that the pain was ischemia and is now resovled. Because the pathologist determines the degree of stenosis by dividing the lumen area by the total area, the degree of stenosis will be overestimated. The i nitial hs troponin I returned 75%.
Coronary Intravascular Ultrasound (IVUS) equipment consists of an IVUS catheter, pullback device and the imaging console. In the geometry, the size of the plaque, its relationship to luminal stenosis, arterial remodeling and eccentricity can be evaluated. Incomplete stent apposition can be detected by intravascular ultrasound.
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. Or is it a very tight stenosis that does not allow enough flow to perfuse myocardium that has a high oxygen demand from severely elevated BP?
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?
This suggests diffuse subendocardial ischemia. However, along with that subendocardial ischemia, there is also STE in lead III with reciprocal ST depression in aVL, and some STE in V1. If there is also subendocardial ischemia, the ST depression vector remains leftward, with a reciprocal ST Elevation vector also to the right.
Contrary to what Ken stated, the ST vector remains mostly posterior __ What about subendocardial ischemia? Subendocardial ischemia results in ST depression, but unfortunately, and rather mysteriously, it does not localize to the ischemic wall. Similarly, STD in aVL is usually reciprocal to inferior ST elevation, not "lateral ischemia."
Angiography : LMCA — 90-99% osteal stenosis. LCx — 50-69% stenosis of the 1st marginal branch; with 100% distal LCx occlusion. There is no definite evidence of acute ischemia. (ie, Simply stated — t he patient was having recurrent PMVT without Q Tc prolongation, and without evidence of ongoing transmural ischemia. (
This suggests further severe ischemia. Even in patients whose moderate stenosis undergoes thrombosis, most angiograms show greater than 50% stenosis after the event. However, one can certainly imagine that many thromboses of non-obstructive lesions completely lyse and do not leave a stenosis on same day or next day angiogram.
His response: “subendocardial ischemia. History sounds concerning for ACS (could be critical stenosis, triple vessel), but differential also includes dissection, GI bleed, etc. Smith : It should be noted that, in subendocardial ischemia, in contrast to OMI, absence of wall motion abnormality is common. Anything more on history?
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. The patient had a critical LAD stenosis. greater than 23.4 is likely anterior STEMI).
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. Culprit, stented) 3.
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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.
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. I did not have more information at the time. To the ED providers, the patient denied CP, SOB, or drug use.
A bedside ultrasound was done by the emergency physician, using Speckle Tracking. Is there likely to be fixed coronary stenosis that led to demand ischemia during pneumonia? --Was Was the ST elevation due to transient demand ischemia, or is it false positive? Unfortunately, that video is unavailable.
Ischemic ST-Segment Depression Maximal in V1-V4 (Versus V5-V6) of Any Amplitude Is Specific for Occlusion Myocardial Infarction (Versus Nonocclusive Ischemia). 90% stenosis of the proximal ramus intermedius, pre procedure TIMI II flow The ramus intermedius is a normal variant on coronary anatomy that arises between the LAD and LCX.
Angiogram showed a critical LAD thrombotic stenosis. The patient went to cath and had a distal LAD 99% stenosis with thrombus and TIMI-2 flow. 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. He underwent CABG.
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). Case continued EMS immediately transported, activated the cath lab and gave 324 mg aspirin en route.
Aortic Dissection, Valvular (especially Aortic Stenosis), Tamponade. 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.
I suspect pulmonary edema, but we are not given information on presence of B-lines on bedside ultrasound, or CXR findings. The patient was started on heparin for possible NSTEMI vs demand ischemia. Smith : "decompensation" of aortic stenosis might have initiated this entire cascade. What "initiates" the aortic stenosis cascade?
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