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He was started on a heparin drip and CTA of the chest was ordered to rule out pulmonaryembolism. This is a case like many others posted (see list below) and the EKG from the patient’s original presentation can be quickly recognized as diagnostic for pulmonaryembolism. In fact, Kosuge et al. Accessed May 28, 2024.
mm has been described in normal subjects) Overall impression: In my opinion and experience, this ECG most likely represents a normal baseline ECG, but with a small chance of pericarditis instead. I texted this to Dr. Smith without any information, and this was his reply: "This could be pericarditis but probably is normal variant."
Here is his initial ED ECG: The R-wave in V4 extends to 33 mm, the computerized QTc is 372 ms The only available previous ECG is from one year ago, during the admission when he was diagnosed with pericarditis: 1 year ago ECG, with clinician and computer interpretatioin of pericarditis Normal 0 false false false EN-US X-NONE X-NONE What do you think?
We have seen this pattern in many pts with acute right heart strain on this blog. __ Smith : The combination of T-wave inversion in V1-V3 and in lead III is very specific for acute pulmonaryembolism. Acute pulmonaryembolism was confirmed on CT: The patient did well with treatment. Now another, with ultrasound.
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 pulmonaryembolism and started on therapeutic anticoagulation. Despite empiric bronchial artery embolization, hemoptysis persisted.
The morphology of V2-V4 is very specific in my experience for acute right heart strain (which has many potential etiologies, but none more common and important in EM than acute pulmonaryembolism). CT angiogram showed extensive saddle pulmonaryembolism. He had multiple cardiac arrests with ROSC regained each time.
The combination of findings consistent with acute coronary occlusion in the anterior and inferior leads is likely due to a large "wraparound" LAD occlusion, should not be confused with the "diffuse" ST elevation of pericarditis, and will usually show reciprocal ST depression in aVL.
They include myocardial ischemia, acute pericarditis, pulmonaryembolism, 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 pulmonaryembolism. 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.
CT pulmonary angiogram was negative for pulmonaryembolism. If the patient continues to have reperfusion, then we would expect progressive terminal T wave inversion then full T wave inversion over time in the future ECGs. Second troponin T resulted at 1,318 ng/L. Chest x-ray was read as normal. Heparin was started. Reocclusion!
In this ECG Cases blog we look at 10 cases of patients with chest pain, including false positive STEMI, false negative STEMI, and other causes to help hone your ECG interpretation skills in time-sensitive cases where those very ECG skills might save a life.
The initial computer and final cardiology interpretation was a differential: “ST elevation, consider early repolarization, pericarditis, or injury.” But STEMI criteria ignore all this and look at ST segments in isolation. Based on STEMI criteria and unhelpful computer interpretation, the patient was rushed to the cath lab.
Smith : This is classic for pulmonaryembolism (PE). Acute pulmonaryembolism was confirmed on CT angiogram: The patient did well. Dyspnea, Chest pain, Tachypneic, Ill appearing: Bedside Cardiac Echo gives the Diagnosis 31 Year Old Male with RUQ Pain and a History of Pericarditis. Vitals were within normal limits.
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