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So this NSTEMI was likely a STEMI(-)OMI with delayed reperfusion. The patient was admitted as ‘NSTEMI’ which is supposed to represent a non-occlusive MI, but the underlying pathophysiology is analogous to a transient STEMI. See these posts: Chest Pain, ST Elevation, and an Elevated Troponin: Should we Activate the Cath Lab?
In SCAPE (sympathetic crashing acute pulmonary edema), Emergency providers seem now to regularly give high dose NTG, but when the BP is 170/105 in a patient who is not crashing, we often fail to give something to lower afterload. __ Here are some Images: The red circle shows the LAD coursing down the anterior interventricular sulcus.
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. TIMI-0 flow.
large ASD, partial anomalous pulmonary venous return, significant tricuspid regurgitation, carcinoid valvular disease, etc,) 2) Conditions causing pressure overload of the RV. Any cause of pulmonary hypertension. Troponin T peaked at 2074 ng/L (very high, typical of OMI/STEMI). The LV EF was 57% at formal echo.
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?
LAD plaque with 0-25 percent stenosis. No signs for aortic dissection or pulmonary embolus. --"Results were discussed with the ordering physician. The LAD has moderate 40% ostial-proximal LAD stenosis and severe 90% mid LAD stenosis involving first diagonal branch. --The Transient STEMI is at high risk of re-occlusion.
The "criteria" for posterior STEMI are 0.5 Is it STEMI or NonSTEMI? The patient had no hypertension, no tachycardia, a normal hemoglobin, no drug use, no hypotension/shock, no murmur of aortic stenosis. Patients with ACS and acute pulmonary edema 3. The troponin I returned at 4.1 mm STE in one lead. This includes: 1.
Smith : there is some minimal ST elevation in V2-V6, but does not meet STEMI criteria. Transient STEMI has been studied and many of these patients will re-occlude in the middle of the night. The estimated pulmonary artery systolic pressure is 27 mmHg + RA pressure. Is it normal STE? This is a "Transient OMI".
This meets "STEMI criteria" However, there is very high voltage, with a very deep S-wave in V2 and tall R-wave in V4. The morphology is not right for STEMI. My interpretation: LVH with secondary ST-T abnormalities, exaggerated by stress, not a STEMI. This is very good evidence that the ST elevation is not due to STEMI.
Clinical Course The paramedic activated a “Code STEMI” alert and transported the patient nearly 50 miles to the closest tertiary medical center. A transthoracic echocardiogram showed an LV EF of less than 15%, critically severe aortic stenosis , severe LVH , and a small LV cavity. Look at the aortic outflow tract. What do you see?
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.
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.
ECG read as: "Shows T wave inversions in the inferior leads and less than 1mm STE in V2, without STEMI criteria." CT pulmonary angiogram was negative for pulmonary embolism. Normal RV, no significant valvular stenosis or regurgitation. All very very subtle. Aspirin was given. Second troponin T resulted at 1,318 ng/L.
I knew that, if the patient had presented with chest discomfort, that this ECG is diagnostic of inferior posterior OMI, even though it is not a STEMI. The ACC/AHA guidelines mandate less than 2 hours cath for patients with ACS with refractory pain, pulmonary edema, or electrical or hemodynamic instability.
They found non-obstructive CAD, with only a 20% stenosis of OM2 and 10% RCA. Patients with pulmonary embolism or aortic dissection who have normal variant ST elevation are at high risk of being diagnosed with pericarditis when what they have is far more serious!! No acute culprit. He was admitted to cardiology. Pericarditis?
CT pulmonary angiogram (unnecessary, often done while missing OMI) was unremarkable. Angiogram around 9am: Culprit lesion mid LAD 100% stenosis TIMI 0 TIMI 3 after PCI Severe apical dyskinesis, severe anteroapical akinesis. Triage ECG: And here she explains her assessment: The ECG was read as simply "No ST elevation." Which is true.
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.
When total LM occlusion does present with STE in aVR, there is ALWAYS ST Elevation elsewhere which makes STEMI obvious; in other words, STE is never limited to only aVR but instead it is part of a massive and usually obvious STEMI. All are, however, clearly massive STEMI. This is her ECG: An obvious STEMI, but which artery?
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?
The cath lab was deactivated by cardiologist on arrival at ED because it was "not a STEMI". No pulmonary embolism is identified. First obtuse marginal also had an 80% stenosis and was stented. Pt received 324 ASA and 2 sprays of nitro with improvement. Cath lab was activated by EMS and transported emergent."
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