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The patient is female in her 80s with a medical hx of previous MI with PCI and stent placement. She had a single chamber ICD/Pacemaker implanted several years prior due to ventricular tachycardia. Are you confident there is no ischemia? Answer : The ECG above shows a regular wide complex tachycardia. Is this: 1.
This is ischemic ST depression, and could be due to increasing tachycardia, with a heart rate over 130, but that is unlikely given that the patient is now complaining of crushing chest pain and that there was tachycardia all along. They agreed ischemia was likely in the setting of demand given DKA and infection.
In any case, the ECG is diagnostic of severe ischemia and probably OMI. So this could be myocarditis but in my opinion needs an angiogram before making that diagnosis. == Dr. Nossen Comment/Interpretation: Evaluation of ischemia on an ECG can be very challenging. Concordant STE of 1 mm in just one lead or 2a.
Precordial ST depression may be subendocardial ischemia or posterior STEMI. Notice there is tachycardia. I have warned in the past that one must think of other etiologies of ischemia when there is tachycardia. The OM-1 was opened and stented, then the LAD was stented 3 days later. There is no ST elevation.
An EKG was repeated around midnight: By itself, this ECG is not diagnostic of anything besides sinus tachycardia, and could be called normal (although there is ST segment straightening in the anterior leads, which should always prompt suspicion). The conventional computer algorithm called “ sinus tachycardia, otherwise normal EKG ”.
A prehospital “STEMI” activation was called on a 75 year old male ( Patient 1 ) with a history of hyperlipidemia and LAD and Cx OMI with stent placement. Whether these EKGs show myocarditis, a normal variant, or something else, they are overall not typical of transmural ischemia of the anterior or high lateral walls. It was stented.
Prior ECG available on file from 2 months before: We do not know the clinical events happening during this ECG, but there is borderline tachycardia, PVCs, and likely some evidence of subendocardial ischemia with small STDs maximal in V5-6/II, slight reciprocal STE in aVR. Culprit lesion was reduced to 0% and stented.
The ECG was incorrectly interpreted as no signs of ischemia. Artificial intelligence can be trained to recognize subtle OMI = My Comment by K EN G RAUER, MD ( 2/6 /2023 ): = The initial ECG in today's case was incorrectly interpreted as, "No signs of ischemia". There is sinus tachycardia at 100-105/minute.
These findings are concerning for inferior wall ischemia with possible posterior wall involvement. Slow TIMI 2 initially with brisk flow status post percutaneous coronary intervention with 18mm drug-eluting stent. C linically — the rhythm we see in the long lead II of ECG #3 behaves similar to MAT, even though there is no tachycardia.
In some cases the ischemia can be seen "through" the flutter waves, whereas in other cases the arrhythmia must be terminated before the ischemia can be clearly distinguished. 2) Tachycardia to this degree can cause ST segment changes in several ways. Again, not an expected outcome with diltiazem).
The patient was referred immediately for cath which revealed RCA occlusion that was stented. Remember, in diffuse subendocardial ischemia with widespread ST-depression there may b e ST-E in lead s aVR and V1. There are well formed R-waves with good voltage/amplitude which is uncommon for ischemia. There is ST depression in V1.
Even though they were passed the 12 hour mark traditionally associated with reperfusion benefits, ongoing ischemia requires emergent angiogram On assessment, the patient appeared uncomfortable, leaning forward in his chair. ACS with refractory ischemia and electrical instability are indications for emergent cath regardless of the ECG!
There is appreciable STE aVR with near-global STD that appropriately maximizes in Leads II and V5, and thus suggesting a circumstance of generic, diffusely populated, circumferential subendocardial ischemia versus occlusive coronary thrombus. [1] STEMI was activated and the patient went to Cath on arrival.
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.
This was stented. If there is polymorphic VT with a long QT on the baseline ECG, then generally we call that Torsades, but Non-Torsades Polymorphic VT can result from ischemia alone. See here for management of Polymorphic Ventricular Tachycardia , which includes Torsades. After pacing, there was no recurrence of Torsades.
Although the shock is no doubt partly a result of poor pump function, with low stroke volume, especially of the RV, it should be compensated for by tachycardia. RCA ischemia often results in sinus bradycardia from vagal reflex or ischemia of the sinus node. He was successfully stented.
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.
He had undergone stenting of the LAD several weeks ago (unclear whether elective for stable symptoms, or in response to acute coronary syndrome). It is a wide complex regular tachycardia at a rate of 120. Is it ventricular tachycardia? It is a wide complex regular tachycardia at a rate of 120. He appeared critically ill.
After stent deployment, we often see improvement in the ST-T within seconds or minutes. Here is the final angiogram following placement of a stent in the ostial RCA. 2:04 PM, post stent deployment You can see that even after complete restoration of flow, the ECG still looks terrible, V most of all.
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