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The patient was transported to the CCU for further medical optimization where a pulmonary artery catheter was placed. DISCUSSION: The 12-lead EKG EMS initially obtained for this patient showed severe ischemia, with profound "infero-lateral" ST depression and reciprocal ST elevation in lead aVR.
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.
And superimposed subendocardial ischemia pattern, of course. Smith's ECG Blog — the presence of an almost “null vector” in standard lead I ( ie, P wave, QRS complex and T wave all under 2mm in size ) — is highly suggestive of longstanding and severe pulmonary disease. She was otherwise very stable during this rhythm.
Either could be a result of myocardial contusion There is some minimal ST depression -- this could represent ischemia What else is there that could use therapy immediately? The estimated pulmonary artery systolic pressure is 49 mmHg + RA pressure. There is a very long ST segment resulting in a very long QT.
Evidence of acute ischemia (may be subtle) vii. Of the 67 patients who underwent targeted tests, suspected diagnoses were confirmed in 49 (73%) patients: aortic stenosis (n = 8, 1%), pulmonary embolism (n = 8, 1%), seizures/stroke (n = 30, 5%), and other diseases (n = 3). Left BBB vi. Pathologic Q-waves viii. LVH or RV d.
For right or wrong reasons, the world of electrophysiology has pushed us into a belief system that, if it is AF, the culprit must be pulmonary veins. In fact, non-pulmonary vein origins can be a staggering 70% in some series. Only 20% of focal AT arise from pulmonary veins. I guess, the same should be true for AF. Reference 1.
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