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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.
There is also STE in lead III with reciprocal depression in aVL and I, as well as some subendocardial ischemia pattern with STD in V5-V6 and STE in aVR. Aslanger's is a combination of acute inferior OMI plus subendocardial ischemia, and due to the ischemia vectors , it has STE only in lead III. Moreover, there is tachycardia.
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.
Bedside cardiac ultrasound showed moderately decreased LV function. CT of the chest showed no pulmonary embolism but bibasilar infiltrates. (And of course Ken's comments at the bottom) An elderly obese woman with cardiomyopathy, Left bundle branch block, and chronic hypercapnea presented hypoxic with altered mental status.
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?
If this STD were due to LVH or to subendocardial ischemia, rather than posterior OMI, it would be maximal in V5 and V6. To me, this looks like pulmonary edema. A bedside ultrasound was done, with dozens of clips, and was even done with Speckle Tracking. B-line predominance bilateral lungs indicates pulmonary edema.
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. The RV was small and IVC empty, making pulmonary embolism extremely unlikely. The RV was small and IVC empty, making pulmonary embolism extremely unlikely.
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. Alternation in ST segment appearance ( or in the amount of ST elevation or depression ) — is often linked to ischemia. She has already had syncope.
Here was his prehospital ECG, which I viewed immediately while the resident performed cardiac ultrasound: What do you think? Here is the cardiac ultrasound which the resident performed as I viewed the ECG: This shows a huge pericardial effusion. Therefore, we performed ultrasound-guided pericardiocentesis. Is is sinus?
There is ST depression beyond the end of the wide QRS in I, II, aVF, and V4-V6, diagnostic of with subendocardial ischemia. A bedside cardiac ultrasound was recorded: Here is a still image of the echo: The red arrows outline the right ventricle and the yellow arrows outline the left ventricle chamber. There is no ST elevation.
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. The rhythm is atrial fibrillation. The QRS complex is within normal limits.
A bedside cardiac ultrasound was normal, with no effusion. and the patient was converted to veno-venous (V-V) ECMO due to persistent pulmonary insufficiency. Use of objective evidence of myocardial ischemia to facilitate the diagnostic and prognostic distinction between type 2 myocardial infarction and myocardial injury.
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. See below.
CT angiogram chest: no aortic dissection or pulmonary embolism. Serial chest xrays: progressive bilateral pulmonary edema. Beware a negative Bedside ultrasound. No further troponins were measured. This gets drilled into them. Chest Pain in a Male in his 20's; Inferior ST elevation: Inferior lead "early repol" diagnosed.
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.
I suspect pulmonary edema, but we are not given information on presence of B-lines on bedside ultrasound, or CXR findings. Anything that causes pulmonary edema: poor LV function, fluid overload, previous heart failure (HFrEF or HFpEF), valvular disease. The patient was started on heparin for possible NSTEMI vs demand ischemia.
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. No acute infectious prodrome, known pulmonary disease, or recent trauma. No prior similar symptoms or known CAD.
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.
Smith : This is classic for pulmonary embolism (PE). Acute pulmonary embolism was confirmed on CT angiogram: The patient did well. See our other acute right heart strain / pulmonary embolism cases: A man in his 50s with shortness of breath Another deadly triage ECG missed, and the waiting patient leaves before being seen.
The clinical significance of ARCA-LCS lies in its potential to cause myocardial ischemia or sudden cardiac death, particularly under physical exertion. Transthoracic echocardiogram, bilateral carotid Doppler ultrasound, and electrocardiogram were normal. A treadmill exercise test revealed ischemic changes.
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