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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.
Alternation in ST segment appearance ( or in the amount of ST elevation or depression ) — is often linked to ischemia. Conduction and refractoriness alternans may be seen with WPW-related as well as AV Nodal-dependent reentr y tachycardias — atrial fibrillation — acute pulmonary embolus — myocardial contusion — and severe LV dysfunction.
He was seen at another hospital and found to have a slightly elevated troponin, then underwent a CT pulmonary angiogram (PE) protocol which revealed a right sided pneumonia. Echo does not necessarily differentiate acute MI from pericarditis: both may have wall motion abnormalities. See an examples of CT ischemia here.
The ECG shows sinus tachycardia with RBBB and LAFB, without clear additional superimposed signs of ischemia. ECG of pneumopericardium and probable myocardial contusion shows typical pericarditis Male in 30's, 2 days after Motor Vehicle Collsion, complains of Chest Pain and Dyspnea Head On Motor Vehicle Collision. ST depression.
The second most common cause of medical cardiac tamponade is acute idiopathic pericarditis. Less common etiologies include uremia, bacterial or tubercular pericarditis, chronic idiopathic pericarditis, hemorrhage, and other causes such as autoimmune diseases, radiation, myxedema, etc.
You do NOT see this in normal variant STE, nor in pericarditis. The only time you see this without ischemia is when there is an abnormal QRS, such as LVH, LBBB, LV aneurysm (old MI with persistent STE) or WPW." Here is the patient's troponin I profile: These were interpreted as due to demand ischemia, or type II MI.
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.
They include myocardial ischemia, acute pericarditis, pulmonary embolism, external compression due to mass over the right ventricular outflow tract region, and metabolic disorders like hyper or hypokalemia and hypercalcemia. According to a recent systematic review and meta-analysis, spontaneous type 1 ECG had 2.4%
CT angiogram chest: no aortic dissection or pulmonary embolism. Serial chest xrays: progressive bilateral pulmonary edema. Pericarditis? No further troponins were measured. Echo: severely dilated LV, severely reduced EF at 10%, severe hypokinesis of LV from mid-apical segments with basal segments better preserved.
The exception is with postinfarction pericarditis , in which a completed transmural infarct results in inflammation of the subepicardial myocardium and STE in the distribution of the infarct, and which results in increased STE and large upright T-waves. These findings together are more commonly seen with pericarditis.
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.
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