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For example, considering whatever symptoms that the patient may have had ( ie, chestpain, palpitations, shortness of breath, etc. ) — what this might mean in view of the ECG we are looking at. STEP #2 = Clinical Impression — in which we correlate our assessment that we made in Step #1 to the clinical situation at hand.
Another ECG was recorded after the nitroglycerine and now without pain: All findings are resolved. This confirms that the pain was ischemia and is now resovled. The history is concerning ( This patient was awakened from sleep by chestpain that persisted for several hours — on a background of intermittent CP in recent weeks ).
There was no chestpain. V1 and V2 are probably placed too high on the chest given close morphological similarity to aVR. More detailed reviews of subendocardial ischemia, as well as acute ECG patterns that breach the typical presentation, can be found here: [link] [link] Imaging revealed no acute head, or spinal, injuries.
No prior exertional complaints of chestpain, dizziness, lightheadedness, or undue shortness of breath. He denied headache or neck pain associated with exertion. I sent this ECG to Dr. Smith, with the only information that it is a 17 year old with chestpain. 24 yo woman with chestpain: Is this STEMI?
The ECLIPSE trial shows that use of IVI to guide coronary stenting in severely calcified lesions prevents death, stent thrombosis, and unplanned repeat procedures in this high-risk patient population. The ECLIPSE trial results were presented at the American College of Cardiology Scientific Session (ACC.25)
A 60-something awoke with 10/10 crushing chestpain. I would expect TIMI-3 flow (normal flow, no persistent ischemia) with a culprit in the RCA (or possibly Circumflex). The angiogram showed an open artery with 95% stenosis and thrombosis and it was stented. He walked in to triage.
A man in his 70s with past medical history of hypertension, dyslipidemia, CAD s/p left circumflex stent 2 years prior presented to the ED with worsening intermittent exertional chestpain relieved by rest. This episode of chestpain began 3 hours ago and was persistent even at rest. For now she can only say Not OMI.
A 70-something female with no previous cardiac history presented with acute chestpain. She awoke from sleep last night around 4:45 AM (3 hours prior to arrival) with pain that originated in her mid back. She stated the pain was achy/crampy. Over the course of the next hour, this pain turned into a pressure in her chest.
This was a male in his 50's with a history of hypertension and possible diabetes mellitus who presented to the emergency department with a history of squeezing chestpain, lasting 5 minutes at a time, with several episodes over the past couple of months. Plan was for admission for chestpain workup. Gottlieb SO, et al.
Written by Pendell Meyers and Peter Brooks MD A man in his 30s with no known past medical history was reported to suddenly experience chestpain and shortness of breath at home in front of his family. Thus, this apparently is Aslanger's Pattern (inferior OMI with single lead STE in lead III, with simultaneous subendocardial ischemia).
This patient, who is a mid 60s female with a history of hypertension, hyperlipidemia and GERD, called 911 because of chestpain. A mid 60s woman with history of hypertension, hyperlipidemia, and GERD called 911 for chestpain. It is also NOT the clinical scenario of takotsubo (a week of intermittent chestpain).
But the symptoms returned with similar pattern – provoked by exertion, and alleviated with rest; except that on each occasion the chestpain was a little more intense, and the needed recovery period was longer in duration. It should be known that each category can easily manifest the generic subendocardial ischemia pattern.
The best course is to wait until the anatomy is defined by angio, then if proceeding to PCI, add Cangrelor (an IV P2Y12 inhibitor) I sent the ECG and clinical information of a 90-year old with chestpain to Dr. McLaren. His response: “subendocardial ischemia. Anything more on history? J Electrocardiol 2013;46:240-8 2.
No chestpain. Normally, concavity in ST segments suggests absence of anterior ischemia (though concavity by itself is not reassuring - see this study ). Later on during the night of his admission he had a short episode of chestpain that resolved with sublingual nitroglycerin. His vitals were initially normal.
Case An elderly patient had acute chestpain and 911 was called. For this analysis, ACO was defined as angiographic evidence of coronary thrombosis with peak cardiac troponin-I (cTn-I) at least 10 ng/mL or cTn-T ≥ 1 ng/ mL. It is important for cardiologists to realize that a paramedic may see something they do not.
There is broad subendocardial ischemia as demonstrated by STE aVR with concomitant STD that almost appears appropriately maximal in Leads II and V5. There is LBBB-like morphology with persistent patterns of subendocardial ischemia. This is the initial ECG: The QRS is widened with a regular cadence, and there are no discernable P waves.
He denied chestpain. Time 7 hours lead reversal There is limb lead reversal (QRS in I and aVL are now inverted), but nevertheless one can see that the ischemia appears to have resolved. Negative trops and negative angiogram does not rule out coronary ischemia or ACS. Next day, with K = 4.6 The evidence of OMI is gone.
It is possible there is microvascular dysfunction producing residual transmural ischemia. But this is most common when there is prolonged ischemia, and this patient had the fastest reperfusion imaginable! He had no chestpain, dyspnea, or any other anginal equivalent, and his vital signs were normal.
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