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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 pulmonary embolism). He had multiple cardiacarrests with ROSC regained each time. CT angiogram showed extensive saddle pulmonary embolism.
Bedside ED ultrasound showed exceedingly poor global LV function, and no B lines. I was there and said, "No, I think this is all due to severe chronic cardiomyopathy and cardiacarrest due to primary ventricular fibrillation, not due to ACS." _ Why did I say that? l/min cardiac output. Here is the initial ED ECG.
Bedside cardiacultrasound showed moderately decreased LV function. CT of the chest showed no pulmonary embolism but bibasilar infiltrates. See this post: How a pause can cause cardiacarrest 2. She was intubated. The plan: 1. Place temporary pacemaker 3. Discontinue amiodarone, since it prolongs the QT 4.
A bedside cardiacultrasound was normal, with no effusion. and the patient was converted to veno-venous (V-V) ECMO due to persistent pulmonary insufficiency. Clinically — despite an initial 2-fold increased troponin, the normal bedside Echo was reassuring against OMI or pulmonary embolism.
The post EM Quick Hits 33 Polytrauma Tips & Tricks, Toxic Megacolon, ECG in PE, Patch Calls, CT Before LP, Nebulized Ketamine appeared first on Emergency Medicine Cases.
A bedside cardiacultrasound 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. It makes pulmonary embolism (PE) very likely. The small LV implies very low LV filling pressures, which implies low pulmonary venous pressure.
Smith comment: before reading anything else, this case screamed pulmonary embolism to me. I would do bedside ultrasound to look at the RV, look for B lines as a cause of hypoxia (which would support OMI, and argue against PE), and if any doubt persists, a rapid CT pulmonary angiogram.
Case Continued Bedside ultrasound was performed: This shows an anterior wall motion abnormality, and highly suggests the LAD as the infarct artery. The patient was slightly tachypneic and mildly hypoxic in the stabilization room and therefore the physicians obtained a CT pulmonary angiogram as well as aortogram to rule out dissection and PE.
Bedside ultrasound showed no effusion and moderately decreased LV function, with B-lines of pulmonary edema. If cardiacarrest from hypokalemia is imminent (i.e., As I indicated above, in our cardiacarrest case, after pushing 40 mEq, the K only went up to 4.2 He was managed medically with Clopidogrel.
I suspect this is Type 2 MI due to prolonged severe hypotension from cardiacarrest. The ways to tell for certain include intravascular ultrasound (to look for extra-luminal plaque with rupture) or "optical coherence tomography," something I am entirely unfamiliar with. pulmonary embolism, sepsis, etc.), myocarditis).
A bedside cardiacultrasound was performed with a parasternal long axis view demonstrated below: There is a large pericardial effusion with collapse of the right ventricle during systole. Cardiac Motion Alternans — is the result of cardiac movement rather than electrical alternation. This patient is only pseudo-stable.
The clinical significance of ARCA-LCS lies in its potential to cause myocardial ischemia or sudden cardiac death, particularly under physical exertion. Transthoracic echocardiogram, bilateral carotid Doppler ultrasound, and electrocardiogram were normal. No previous history of hypertension or diabetes.
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