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This certainly looks like an anterior STEMI (proximal LAD occlusion), with STE and hyperacute T-waves (HATW) in V2-V6 and I and aVL. How do you explain the anterior STEMI(+)OMI immediately after ROSC evolving into posterior OMI 30 minutes later? This caused a type 2 anterior STEMI.
Past medical history included RBBB without other cardiac history, but old ECG was not available. The prehospital and ED computer interpretation was inferior STEMI: There’s normal sinus rhythm, first degree AV block and RBBB, normal axis and normal voltages. Vitals were normal except for oxygen saturation of 94%. Vitals were normal.
Smith interpretation: This is highly likely to be due to extreme right heart strain and is nearly diagnostic of pulmonary embolism. She was diagnosed with a Non-STEMI and kept overnight for a next day angiogram. Medics recorded the above ECG and called a STEMI alert. The patient went into arrest pre-hospital.
Could this be Septal STEMI (STE in V1 and aVR, with reciprocal ST depression in V4-V6?), In Septal STEMI , transmural ischemia of the septum is recorded by the overlying lead V1 as ST Elevation. Lead III is also on the right and might manifest ST Elevation in Septal STEMI. with ADDED STE in III?
This is a troponin I level that is almost exclusively seen in STEMI. I suspect this is Type 2 MI due to prolonged severe hypotension from cardiacarrest. So this is either a case of MINOCA, or a case of Type II STEMI. If the arrest was caused by acute MI due to plaque rupture, then the diagnosis is MINOCA.
A prehospital ECG was recorded (not shown and not seen by me) which was worrisome for STEMI. A previous ECG from 4 years prior was normal: This looks like an anterior STEMI, but it is complicated by tachycardia (which can greatly elevate ST segments) and by the presentation which is of fever and sepsis.
Bedside ultrasound showed no effusion and moderately decreased LV function, with B-lines of pulmonary edema. Here is his ED ECG: There is obvious infero-posterior STEMI. What are you worried about in addition to his STEMI? If cardiacarrest from hypokalemia is imminent (i.e., He appeared to be in shock.
and the patient was converted to veno-venous (V-V) ECMO due to persistent pulmonary insufficiency. In a series of 18 patients with COVID and ST elevation, 8 were diagnosed with STEMI, 6 of whom had an angiogram and it showed obstructive coronary disease. 12 All STEMI patients had very high cTn typical of STEMI (cTnT > 1.0
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.
It makes pulmonary embolism (PE) very likely. The small LV implies very low LV filling pressures, which implies low pulmonary venous pressure. It was a PEA or bradyasystolic arrest , not a shockable rhythm. LV anterior STEMI does not give maximal ST elevation in V1. So this ECG is typical of right ventricular (RV) STEMI.
I've previously discussed the interesting correlation of a qR pattern in lead V1 in patients with RVH — as strongly suggesting associated pulmonary hypertension ( See ECG Blog #234 and Blog #248 ). But limitation of this ST elevation to a single lead is not consistent with any distribution of a STEMI. He could not be resuscitated.
The paramedics diagnosis was "Possible Anterolateral STEMI." Chest X-ray also showed pulmonary edema. More proof that a huge STEMI may have normal or near normal initial troponin. Primary VF in this study refers to fibrillation occurring in the absence of shock or pulmonary edema. She was given 2 mg Magnesium.
A 12-lead was recorded, showing "STEMI," but is unavailable. The patient was unconscious BEFORE the cardiacarrest, at the same time that she had strong pulses. Therefore, cardiacarrest is NOT the etiology of the coma. she had severe pulmonary edema. She was BVM ventilated and suctioned. From this site.
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