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A CT Coronaryangiogram was ordered. Here are the results: --Minimally obstructive coronary artery disease. --LAD No signs for aortic dissection or pulmonary embolus. --"Results were discussed with the ordering physician. A repeat troponin returned at 0.45 ng/mL, consistent with reperfused OMI, or Non-OMI.
Clinical introduction A patient in their 30s had been diagnosed with peripartum cardiomyopathy, pulmonary oedema, with severe left ventricular dysfunction at the seventh month of gestation in the third pregnancy in their late 20s. The coronaryangiogram was normal.
Will you accept this patient for emergent coronaryangiogram based on the ECG changes? Putting all the findings together; dyspnea, slight tachycardia, delayed R-wave progression, prominent lateral S waves and ST depression maximal where the P waves are largest all point toward pulmonary disease as the cause of the ECG findings.
CT of the chest showed no pulmonary embolism but bibasilar infiltrates. Finally, do a coronaryangiogram Possible alternative to pacing is to give a beta-1 agonist to increase heart rate. She was intubated. Bedside cardiac ultrasound showed moderately decreased LV function. Dobutamine is an acceptable alternative.
In SCAPE (sympathetic crashing acute pulmonary edema), Emergency providers seem now to regularly give high dose NTG, but when the BP is 170/105 in a patient who is not crashing, we often fail to give something to lower afterload. __ Here are some Images: The red circle shows the LAD coursing down the anterior interventricular sulcus.
She had idiopathic ventricular fibrillation in 1992, treated with an EPD (Picture 1A), later replaced by a transvenous ICD.She was diagnosed with left femoral deep venous thrombosis and bilateral pulmonary embolism and started on therapeutic anticoagulation. She was transferred to our institution for further evaluation.
On his physical examination, cardiac and pulmonary auscultation was completely normal. Bi-phasic scan showed no dissection or pulmonary embolism. Coronary arteries cannot be assessed because the scan was not gated, but proximal segments of the coronary arteries seem to be open with some contrast.
CT angiogram chest: no aortic dissection or pulmonary embolism. Serial chest xrays: progressive bilateral pulmonary edema. Only after her troponin peaked at 500,000 ng/L did she get her angiogram, which showed a 100% left main occlusion due to ruptured plaque. No further troponins were measured.
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 patient was transported to the CCU for further medical optimization where a pulmonary artery catheter was placed.
Discussion Thus, no further ECGs were recorded and there was no angiogram or stress test or CT coronaryangiogram. P.S.: Keep in mind that competing conditions ( ie, hyperkalemia, acute infarction, conduction defects, pulmonary disease ) may mask ECG diagnosis of LVH. The ECG is simply not optimally accurate.
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. Acute coronary occlusion and acute pulmonary edema can coexist.
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