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Angiogram No obstructive epicardial coronaryarterydisease Cannot exclude non-ACS causes of troponin elevation including coronary vasospasm, stress cardiomyopathy, microvascular disease, etc. Plaque rupture or erosion has been diagnosed by intravascular ultrasound in about 40 percent of women with MINOCA [ 12 ].
Prehospital Conventional algorithm interpretation: ANTERIOR INFARCT, STEMI Transformed ECG by PM Cardio: PM Cardio AI Bot interpretation: OMI with High Confidence What do you think? On arrival, lung ultrasound confirmed pulmonary edema (B lines). Mild Plaque no angiographically significant obstructive coronaryarterydisease.
This has been termed a “STEMI equivalent” and included in STEMI guidelines, suggesting this patient should receive dual anti-platelets, heparin and immediate cath lab activation–or thrombolysis in centres where cath lab is not available. aVR ST segment elevation: acute STEMI or not? Incidence of an acute coronary occlusion.
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.
This is a troponin I level that is almost exclusively seen in STEMI. So this is either a case of MINOCA, or a case of Type II STEMI. If the arrest had another etiology (such as old scar), and the ST elevation is due to severe shock, then it is a type II STEMI. I believe the latter (type II STEMI) is most likely.
Given her risk factors (HTN, HLD, ESRD from diabetes) I decided to obtain a broad cardiac workup for the patient: serial ECGs, labs, serial troponins, CXR and bedside cardiac ultrasound. Ultrasounds can be very helpful in guiding your diagnostic pathway: location of WMA on US led to obtaining posterior leads.
No pericardial effusion on ultrasound." Smith and Meyers to diagnose both obvious (STEMI) and subtle OMI. But the stuttering pain and sudden onset suggest acute coronary occlusion (Occlusion MI, or OMI). "ECG Cath lab activation by the ED and I agree with coronary angiography emergently." What do you think? Medical Rx.
Smith comment: This patient did not have a bedside ultrasound. Had one been done, it would have shown a feature that is apparent on this ultrasound (however, this patient's LV function would not be as good as in this clip): This is recorded with the LV on the right. What should be done? Should the cath lab be activated?
More past history: hypertension, tobacco use, coronaryarterydisease with two vessel PCI to the right coronaryartery and circumflex artery several years prior. He reports that this chest pain feels different than prior chest pain when he had his STEMI/OMI, but is unable to further describe chest pain.
The ECG shows obvious STEMI(+) OMI due to probable proximal LAD occlusion. Studies of patients with coronaryarterydisease who developed arrhythmic storm with episodes of PMVT following MI — show arrhythmias indistinguishable from those reported in this case. The below ECG was recorded.
I suspect pulmonary edema, but we are not given information on presence of B-lines on bedside ultrasound, or CXR findings. Anything that causes pulmonary edema: poor LV function, fluid overload, previous heart failure (HFrEF or HFpEF), valvular disease. Supply-demand mismatch can cause ST Elevation (Type 2 STEMI). Management?
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