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Finally, do a coronaryangiogram Possible alternative to pacing is to give a beta-1 agonist to increase heart rate. This usually done by a pacer lead placed through the coronary sinus (LV venous system). Use Lidocaine instead (lidocaine prevents the PVCs which cause R on T, and does not prolong the QT.)
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. Smith comment 2: I frequently see failure to control BP in patients with acute chest pain or acute heartfailure.
The diagnostic coronaryangiogram identified only minimal coronary artery disease, but there was a severely calcified, ‘immobile’ aortic valve. Aortic angiogram did not reveal aortic dissection. The ECG cannot diagnose the etiology of ischemia; it only the presence of ischemia, from whatever etiology.
There is broad subendocardial ischemia as demonstrated by STE aVR with concomitant STD that almost appears appropriately maximal in Leads II and V5. There is LBBB-like morphology with persistent patterns of subendocardial ischemia. This worried the crew of potential acute coronary syndrome and STEMI was activated pre-hospital.
He was transitioned to oral heartfailure medications and discharged home slightly over one week after presentation. He was readmitted a few weeks later for a heartfailure exacerbation, diuresed, and discharged again. The last information available is that the patient was undergoing heart transplant evaluation.
Anything that causes pulmonary edema: poor LV function, fluid overload, previous heartfailure (HFrEF or HFpEF), valvular disease. The patient was started on heparin for possible NSTEMI vs demand ischemia. increasing stenosis, ischemia, volume changes, increased blood pressure, atrial fibrillation, etc.)
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