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Intermediate-risk patients may be further stratified based on recent stress testing or coronary angiogram findings plus a modified HEART or Emergency Department Assessment of Chest Pain (EDACS) score. The patient has no previous stress testing or coronary angiogram, and he is not low risk by HEART or EDACS scoring.
What would you do at this time with this information? But pain is an important signal in MI and informs the clinician of the urgency. For the same reason, you should not delay coronary angiography because pain resolves with morphine. But pain is a critical signal for urgency in the context of acute coronary syndrome.
If this EKG were handed to you to screen from triage without any clinical information, what would you think? Electrocardiographic Differentiation Between Acute Pulmonary Embolism and Acute Coronary Syndromes on the Basis of Negative T Waves - ScienceDirect. looked at consecutive patients with PE, ACS, or neither. Kosuge et al.
This was texted to me from a former resident, while working at a small rural hospital, with the statement: "I can’t convince myself of anything here, but he’s a 63-year-old guy with prior stents and a good story for ACS." We don't know if he had a stress test, a CT Coronary angiogram, or they just decided to do an angiogram.
If there were diffuse ischemic STD, with precordial STDmaxV5-6 and reciprocal STE-aVR, this would be non-specific subendocardial ischemia from ACS or supply-demand mismatch. The new ESC guidelines has for the first time merged both STEMI and non-STEMI in the same guideline because they are both on the spectrum of ACS.
ACS would be highly unusual in a young athlete, and given the information on his race bib, one must first suspect that the abnormal ST elevation is due to demand ischemia, not ACS. The next day, and angiogram showed normal coronary arteries. Now there is much less ST segment deviation, less elevation and less depression.
More past history: hypertension, tobacco use, coronary artery disease with two vessel PCI to the right coronary artery and circumflex artery several years prior. This is diagnostic of ACS; it appears to be a reperfused acute inferior OMI. It is unknown when this pain recurred and became constant.
At this point, with the information above, the patient's overall clinical picture could be consistent with either reperfused OMI, or Non-OMI, since both may have absent pain and inverted T waves. A CT Coronary angiogram was ordered. Here are the results: --Minimally obstructive coronary artery disease. --LAD
There were zero patients in this study with a "normal" ECG who had any kind of ACS! Old ‘NSTEMI’ A history of coronary artery disease and a stent to the same territory further increases pre-test likelihood of acute coronary occlusion, including in-stent thrombosis. So this study is actually worthless.
Written by Pendell Meyers Both of these cases were sent to me with no information other than adults with acute chest pain. What would be your response? Case 1: Case 2: What if I told you that Case 1 has an abnormal initial troponin, and Case 2 has a normal initial troponin? Case 1 An elderly male presented with chest pain.
Learning points: Both patients and other medical providers can report confusing and often contradictory information that obfuscates the diagnosis (in this case, WPW). Serial ECGs enhance the diagnosis of acute coronary syndrome. If the story and ECG findings are concerning, use your clinical judgment to advocate for PCI. Washam, J.
Distilling this case into its most salient components, a man with multiple risk factors for coronary disease is presenting with several days of chest pain and markedly elevated troponin with no other reason to explain the lab abnormality ( e.g. sepsis). The patient has ACS by history, active pain, and an elevated troponin.
Smith: If this is ACS (a big if), t his is just the time when one should NOT use "upstream" dual anti-platelet therapy ("upstream" means in the ED before angiography). History sounds concerning for ACS (could be critical stenosis, triple vessel), but differential also includes dissection, GI bleed, etc. Anything more on history?
I texted this ECG with no information to Dr. Smith, who immediately said: "If CP, then anterior OMI until proven otherwise." References: 1) See this study showing an association between morphine and mortality in Non-STE-ACS: Meine TJ, Roe M, Chen A, Patel M, Washam J, Ohman E, Peacock W, Pollack C, Gibler W, Peterson E. Am Heart J.
However, vertical flow can result in myocardial injury secondary to coronary artery spasm. This is supplied via alternating current (AC), increasing the risk of titanic contraction of skeletal muscle, leading to kids holding on to the electrical power source. AC and DC shocks may result in different injury patterns.
We who know ischemic ECGs know that really when T-wave inversion is specific for coronary thrombosis that it indicates reperfusion of the artery, not active occlusion. that is, show a pattern of labile ST-T wave changes not due to an acute coronary event. I personally can hardly wait for that future version! Some patients do this.
I saw this before any other information and knew immediately that it represented an LAD occlusion. Now you have ECG and troponin evidence of ischemia, AND ventricular dysrhythmia, which means this is NOT a stable ACS. What is Spontaneous Coronary Artery Dissection (SCAD)? Here was her ECG at time zero: What do you think?
The fire department, who operate at an EMT level in this municipality, arrived before us and administered 324 mg of baby aspirin to the patient due to concern for ACS. Such cases are classified as MINOCA (Myocardial Infarction with Non-Obstructed Coronary Arteries). An angiogram is a "lumenogram;" most plaque is EXTRALUMINAL!!
An ECG was texted to me (Smith) without any clinical information: What did I say? This clinical information followed: "The patient had a COPD exacerbation with a prehospital SpO2 of 60%. This clinical information followed: "The patient had a COPD exacerbation with a prehospital SpO2 of 60%. This is NOT Wellens. Kosuge et al.
With no other information other than the first ECG above, I texted this to Dr. Smith and he responded: ST elevation in lead V2 and terminal QRS distortion in V3. See this study showing an association between morphine and mortality in ACS: Use of Morphine in ACS is independently associated with mortality, at odds ratio of 1.4
Here is his triage ECG: PM Cardio version: With no other information at all, I sent this ECG to Dr. Smith, who replied: "I think it is real. ST depression maximal in V1-V4, in the context of ACS symptoms and unexplained by QRS abnormality or tachydysrhythmia, should be considered posterior OMI until proven otherwise. STD in V4-5 too."
Remember that the ECG reports what is happening to the myocytes , then you must use that information to make inferences about what the patient needs. Acute coronary occlusion is the most common and most treatable cause of this pattern, but it is not the only cause. This ECG can never be a baseline ECG.
The ECG is diagnostic for acute transmural infarction of the anterior and lateral walls, with LAD OMI being the most likely cause (which has various potential etiologies for the actual cause of the acute coronary artery occlusion, the most common of which is of course type 1 ACS, plaque rupture with thrombotic occlusion).
After rethinking the case, he remained concerned about ACS and subsequently performed a point-of-care ultrasound in order to evaluate for regional wall motion abnormality. We do not know whether a better assay would have given better information, but it is very likely. There is no age cut-off for ACS. Do NOT use them.
If this is ACS with Aslanger's pattern , the ST depression vector of subendocardial ischemia (due to simultaneous 3 vessel or left main ACS) is directed toward lead II (inferior and lateral). Thus, this apparently is Aslanger's Pattern (inferior OMI with single lead STE in lead III, with simultaneous subendocardial ischemia).
I did not have more information at the time. I remained unconvinced that this was due to ACS. With the added history, and the entirety of the presentation, it was determined by cardiology that the clinical presentation was not due to ACS. Is there a formula to help with this? See discussion at the bottom.
Evaluate and treat seizures or SE after CA in the context of other available clinical information because other systemic factors may influence the occurrence of seizures or SE and the effectiveness of treatment (90%, 18/20). The treatment goal for post-CA SE is seizure suppression or burst suppression for a minimum of 24 hours (95%, 19/20).
Fortunately, Dr. Cho was not looking for STEMI ECG criteria but for an acute coronary occlusion. As he documented, “This patient is experiencing chest pain consistent with an acute coronary syndrome. Start using the terms acute coronary occlusion and occlusion MI. That’s exactly what happened in this case.
A 68-year-old male with a past medical history of hypertension, diabetes mellitus, and coronary artery disease with a drug eluting stent placed 2 months ago presents with dizziness and vomiting that began 3 hours ago. The NIHSS cutoff that predicts outcomes is 4 points higher in AC compared with PC infarctions.
Written by Pendell Meyers I was reading ECGs in a database (without any clinical information) when I came to this one: What do you think? You must understand this and the dynamic nature of ACS to provide excellent care for such patients. Seeing only this ECG with no context, I thought this ECG was within normal limits.
Corroborating this is the subtle ST depression in V2-V3 which is inappropriate for the normal QRS complex, and in the context of ACS, we have shown this is quite specific for posterior OMI. I sent the ECG with no information to Dr. McLaren, who instantly replied: "RCA?" (he he means, "inferoposterior OMI, so probably RCA occlusion?").
I sent this to Dr. Meyers without any other information, and he responded, “do you have a prior to make sure that it is all just because of the delta wave? The emergency physician wasn’t sure what to make of the changes from one ECG to the next but was concerned about ACS. What do you think? What do you think?
Recall that, in the setting of ACS symptoms, ST depression that are maximal in leads V1-V4 (as opposed to V5 and V6) not attributable to an abnormal QRS complex is specific for OMI. Optimal treatment for today's patient would have been prompt cath with PCI to the "culprit" artery with the goal of maintaining coronary perfusion.
The axiom of "type 1 (ACS, plaque rupture) STEMIs are not tachycardic unless they are in cardiogenic shock" is not applicable outside of sinus rhythm. This case represents the same physiologic event as OMI in terms of the result on the myocardium, therefore with identical ECG features, however there may not be ACS!
Written by Pendell Meyers A man in his late 40s with several ACS risk factors presented with a chief complaint of chest pain. I texted this to Dr. Smith without any information, and this was his reply: "This could be pericarditis but probably is normal variant." Our THANKS to Dr. Meyers for presenting this informative case!
He had no symptoms of ACS. greater than 40mS, V1-V2" Meyers interpretation: I was sent this ECG with no clinical information whatsoever, and I responded: "Easily diagnostic of acute LAD occlusion." His HEAR score (before troponin resulted) was documented at 3, with documentation stating "low suspicion for ACS."
Just so you know this ECG interpretation is not done by the retrospectoscope: I sent it to Dr. Smith without any information, and he immediately responded: "Infero-postero-lateral OMI" The ECG had a computer and final cardiology interpretation of “possible inferior infarct, age undetermined”, because of Q waves.
And so it is wise to look at the coronary arteries. This ECG certainly looks like myocarditis, and was due to myocarditis, but missing acute coronary occlusion is not acceptable. 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.
This ECG was texted to me with no information: I answered: "Show me the whole 12-lead." There was no ACS here. Discussion On this blog, I show a lot of ECGs that were sent to me and show subtle findings of OMI (acute coronary occlusion). And it turns out that this was the baseline ECG.
I sent this "normal" ECG without any information to a number of ECG enthusiasts, who were all concerned about possible OMI - whether subtle high lateral OMI with inferior reciprocal change, or subtle inferior OMI with high lateral reciprocal change. Take home 1. C ircumflex occlusions can have subtle to no ECG changes 3.
If she had no risk factors, it is doubtful that she would have developed such extensive coronary artery disease as we see on the angiogram. However, this additional information was supportive. Patients like her are the reason we are advocating for a change in the ACS paradigm from STEMI to OMI.
Meyers : This ECG was texted to me with no clinical information, and my response was: "That looks like a very subtle LAD OMI. This is a h igher - p revalence H istory for acute coronary disease. Very very subtle one. What happened?" Descriptive Analysis of E CG # 1 : The rhythm is sinus at ~85/minute.
Here is a video lecture of subtle LAD occlusion: One hour lecture on Subtle ECG Findings of Coronary Occlusion The 3-variable formula comes from this paper: Smith SW et al. Case 3 I was reading a stack of ECGs yesterday, and saw this one, with no clinical information. 4-variable version still to come. Go here to find excel applets.
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