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We present the case of a man in his 50s, admitted with cardiacarrest secondary to inferolateral STEMI. Successful PPCI was performed via right femoral artery, with access gained under ultrasound guidance.
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. A list of conditions that can cause this is below.
On arrival, the patient was in shock, was intubated, and had an immediate cardiacultrasound. What does a heart look like on ultrasound when the EKG looks like that? Here you go: It's not the world's greatest cardiacultrasound video, but it does appear to show poor function and low volume. How would you treat?
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. She was defibrillated and resuscitated. ng/mL [IQR: 0.46, 2.35].
Aslanger added in the limitations in his article: " Theoretically, an isolated basal inferoseptal infarction or an acute inferior MI in the presence of previous infarctions that may change the orientation of lesion vector can also cause a similar picture. Could this be Septal STEMI (STE in V1 and aVR, with reciprocal ST depression in V4-V6?),
He had a previous MI with cardiacarrest 2 years prior. There was an old ECG for comparison: One year prior with no ST segment abnormalities A bedside cardiacultrasound was done by the emergency physician. Case A 47 year old male called 911 for severe chest pain. He was clammy and looked unwell.
A bedside cardiacultrasound was normal, with no effusion. 4 Unfortunately, this article provides no electrocardiographic, echo, or angiographic data, so it is not certain that these high levels were in the absence of acute MI. He had the following EKG recorded: Low voltage, suggests effusion.
Bedside ultrasound showed no effusion and moderately decreased LV function, with B-lines of pulmonary edema. If cardiacarrest from hypokalemia is imminent (i.e., However, this review references the Sterns article above, which by my reading does not state this. He was managed medically with Clopidogrel. mEq/L, from 1.9
Another approach is sympathetic chain (stellate ganglion) blockade if you have the skills to do it: it requires some expertise and ultrasound guidance. baseline (this is what most recommend but seems like far too much QRS widening to me) = See these articles and this graphic: 1.
Further history later: This patient personally has no further high risk features (syncope / presyncope), but her mother had sudden cardiacarrest in sleep. A bedside cardiacultrasound revealed grossly normal to hyperdynamic systolic function with no obvious areas of wall motion abnormalities.
On arrival in the ED, a bedside ultrasound showed poor LV function (as predicted by the Queen of Hearts) with diffuse B-lines. We showed this in this article in JAMA Cardiology. A retrospective 'target trial emulation' comparing amiodarone and lidocaine for adult out-of-hospital cardiacarrest resuscitation.
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