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There is also STE in lead III with reciprocal depression in aVL and I, as well as some subendocardial ischemia pattern with STD in V5-V6 and STE in aVR. Aslanger's is a combination of acute inferior OMI plus subendocardial ischemia, and due to the ischemia vectors , it has STE only in lead III. Moreover, there is tachycardia.
Bedside cardiac ultrasound showed moderately decreased LV function. CT of the chest showed no pulmonary embolism but bibasilar infiltrates. (And of course Ken's comments at the bottom) An elderly obese woman with cardiomyopathy, Left bundle branch block, and chronic hypercapnea presented hypoxic with altered mental status.
ET Main Tent (Hall B1) This session offers more insights from key clinical trials presented at ACC.24 24 and find out what it all means for your patients.
My opinion was that it was not a cath lab case, but I did suggest they do a bedside ultrasound to look for an anterior wall motion abnormality. The RV was small and IVC empty, making pulmonary embolism extremely unlikely. The RV was small and IVC empty, making pulmonary embolism extremely unlikely.
This suggests further severe ischemia. The problem is difficult to study because angiographic visualization of arteries is not perfect, and not all angiograms employ intravascular ultrasound (IVUS) to assess for unseen plaque or for plaque whose rupture and ulceration cannot be seen on angiogram. And yet the arteries remain open.
This case was provided by Spencer Schwartz, an outstanding paramedic at Hennepin EMS who is on Hennepin EMS's specialized "P3" team, a team that receives extra training in advanced procedures such as RSI, thoracostomy, vasopressors, and prehospital ultrasound. Takotsubo is a sudden event, not one with crescendo angina.
There is ST depression beyond the end of the wide QRS in I, II, aVF, and V4-V6, diagnostic of with subendocardial ischemia. A bedside cardiac ultrasound was recorded: Here is a still image of the echo: The red arrows outline the right ventricle and the yellow arrows outline the left ventricle chamber. There is no ST elevation.
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.
A bedside cardiac ultrasound was normal, with no effusion. Use of objective evidence of myocardial ischemia to facilitate the diagnostic and prognostic distinction between type 2 myocardial infarction and myocardial injury. He had the following EKG recorded: Low voltage, suggests effusion. Available from: [link] 9.
CT angiogram chest: no aortic dissection or pulmonary embolism. Beware a negative Bedside ultrasound. He spent several days in the PICU, undergoing workup including: Serial troponins: rising from 5,700 ng/L (unknown if I or T) to greater than 25,000 ng/L (greater than the lab's upper limit of reporting). Pericarditis?
Check : [vitals, SOB, Chest Pain, Ultrasound] If the patient has Abdominal Pain, Chest Pain, Dyspnea or Hypoxemia, Headache, Hypotension , then these should be considered the primary chief complaint (not syncope). Evidence of acute ischemia (may be subtle) vii. Aortic Dissection, Valvular (especially Aortic Stenosis), Tamponade.
Case continued A bedside cardiac ultrasound revealed grossly preserved left ventricular function, no appreciable wall motion abnormality, pericardial effusion, or obvious valvular abnormality. A good size infarct that no longer has active ischemia will have continually rising troponins due to the damage that was done hours ago.
Smith : This is classic for pulmonary embolism (PE). Acute pulmonary embolism was confirmed on CT angiogram: The patient did well. See our other acute right heart strain / pulmonary embolism cases: A man in his 50s with shortness of breath Another deadly triage ECG missed, and the waiting patient leaves before being seen.
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