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Many of the changes seen are reminiscent of LVH with “strain,” and downstream Echo may very well corroborate such a suspicion, but since the ECG isn’t the best tool for definitively establishing the presence of LVH, we must favor a subendocardial ischemia pattern, instead. The CXR demonstrated no pulmonary edema. Type I ischemia.
This EKG is diagnostic of transmural ischemia of the inferior wall. The scan also showed “scattered coronary artery plaques”. __ Smith comment 1 : the appropriate management at this point is to lower the blood pressure (lower afterload, which increases myocardial oxygen demand). Lead I also shows reciprocal ST depression.
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.
Coronary Artery Disease (CAD) CAD, which involves the narrowing or blockage of coronary arteries due to plaque buildup, can reduce blood flow to the heart. This may result in ischemia (lack of oxygen to the heart muscle), causing parts of the heart to weaken and enlarge.
Source: JAMA Cardiology) Patients with afib who survived an intracerebral haemorrhage had a very significant risk of cerebrovascular ischemia episodes and death in the following year, according to registry data. JACC: Asia) Lexaria Bioscience has announced that a CBD product beats a placebo in simulating acute pulmonary hypertension.
PAD is a serious, progressive cardiovascular disease primarily caused by a buildup of fatty plaque in the blood vessels, or atherosclerosis. This plaque narrows the blood vessels and reduces blood flow to the legs and feet, which may significantly impair physical function, walking performance and quality of life.
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.
From there, the right ventricle pumps the blood to the lungs via the pulmonary arteries for reoxygenation. Additionally, the heart’s high demand for oxygen makes it particularly vulnerable to conditions like ischemia (reduced blood flow), which can weaken or damage the heart muscle if left untreated.
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.
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. The septum appears a bit darker than the rest, and you might be fooled into thinking there is ongoing ischemia here. See an examples of CT ischemia here.
Bedside POCUS showed very poor LV function and a few pulmonary B lines. A Chest X-ray did not show pulmonary edema. Time 7 hours lead reversal There is limb lead reversal (QRS in I and aVL are now inverted), but nevertheless one can see that the ischemia appears to have resolved. He was put on BiPAP. Next day, with K = 4.6
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