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Many of the changes seen are reminiscent of LVH with “strain,” and downstream Echo may very well corroborate such a suspicion, but since the ECG isn’t the best tool for definitively establishing the presence of LVH, we must favor a subendocardial ischemia pattern, instead. The CXR demonstrated no pulmonary edema. Type I ischemia.
This EKG is diagnostic of transmural ischemia of the inferior wall. If it is angina, lowering the BP with IV Nitroglycerine may completely alleviate the pain and the (unseen) ECG ischemia. Or is it a very tight stenosis that does not allow enough flow to perfuse myocardium that has a high oxygen demand from severely elevated BP?
Such a pattern is consistent with significant left main coronary artery stenosis. Clinical evaluation and X-Ray chest showed features of pulmonary edema. Angiography done after initial stabilization showed severe stenosis of distal left main coronary artery. ST segment elevation is noted in aVR.
This suggests diffuse subendocardial ischemia. However, along with that subendocardial ischemia, there is also STE in lead III with reciprocal ST depression in aVL, and some STE in V1. If there is also subendocardial ischemia, the ST depression vector remains leftward, with a reciprocal ST Elevation vector also to the right.
A transthoracic echocardiogram showed an LV EF of less than 15%, critically severe aortic stenosis , severe LVH , and a small LV cavity. The patient was transported to the CCU for further medical optimization where a pulmonary artery catheter was placed. If you see this, you should Doppler the valve.
There is normal R-wave progression in the precordial leads with no evidence of ischemia. 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. What do you think?
This usually represents posterior OMI, but in tachycardia and especially after cardiac arrest, this could simply be demand ischemia, residual subendocardial ischemia due to the low flow state of the cardiac arrest. This rules out subendocardial ischemia and is diagnostic of posterior OMI. V4-5 continue to show STD. TIMI-0 flow.
--The STD in V2-V6 might be interpreted as subendocardial ischemia, but with the inferior STE, it is far more likely to represent posterior OMI. In subendocardial ischemia, cath lab is indicated if the pain persists in spite of medical therapy (aspirin, anticoagulant, IV nitro). At 100 minutes, the above ECG was recorded.
remain hypo- or akinetic for some time even if not infarcted, just due to the profound ischemia incurred during the occlusive phase. Thus, an acute wall motion abnormality is not a sign of active or persistent ischemia, and thus is not necessarily an indication for emergent cath. Even many NOMI have wall motion abnormalities.
Low LV filling pressures are due to several etiologies, most commonly due to volume depletion (dehydration or hemorrhage), but also due to other etiologies including, but not limited to: mitral stenosis, pulmonary hypertension (chronic, or due to pulmonary embolism), or poor RV performance.
But when the clinical presentation is sepsis, one must entertain the possibility that the ST elevation is due to demand ischemia, or some other process, and exacerbated by tachycardia. The estimated pulmonary artery systolic pressure is 37 mmHg + RA pressure. Normal estimated left ventricular ejection fraction lower limits of normal.
Part of the ST depression with deep T wave inversion in the lateral chest leads clearly reflects LV "strain" from the marked LVH — but despite the very large QRS amplitudes, this ST-T wave appearance looks disproportionate, suggesting at least a component of ischemia. Then there is the significant ST elevation we see in lead V1.
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.
Post by Smith and Meyers Sam Ghali ( [link] ) just asked me (Smith): "Steve, do left main coronary artery *occlusions* (actual ones with transmural ischemia) have ST Depression or ST Elevation in aVR?" That said, complete LM occlusion would be expected to have subepicardial ischemia (STE) in these myocardial territories: STE vector 1.
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. The patient was started on heparin for possible NSTEMI vs demand ischemia.
Aortic Dissection, Valvular (especially Aortic Stenosis), Tamponade. Evidence of acute ischemia (may be subtle) vii. heart auscultation (aortic stenosis); c. ST segment and T wave abnormalities consistent with or possibly related to myocardial ischemia. 2nd or 3rd degree AV blocks or sinus pause of at least 2 seconds iv.
Watch what happends as the heart recovers from its episode of ischemia. Angiogram: Severe two-vessel coronary artery disease of a left dominant system including 70 to 80% stenosis involving the distal left main/bifurcation. The ECG shows inferior ischemia. Are the T-waves in leads I and II hyperacute? Hard to tell.
August 2024 Approvals Minima Stent System (P240003) (Approval Date: August 28, 2024) The Minima Stent System is an expandable cobalt-chromium metal mesh tube to reopen blood vessels in neonates, infants, and children with Coarctation of the Aorta and Pulmonary Artery Stenosis, specifically designed to expand as younger patients grow.
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