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Overall, this looks like one of the rare ECGs that is actually specific for pericarditis in my opinion. Pericarditis maybe." Meyers' words — "is one of the rare ECGs that is actually specific for pericarditis". ii ) Today's case emphasizes the importance of the history in making the diagnosis of pericarditis.
But there was some doubt as to whether it might be pericarditis because of the ST elevation in I and II, without ST depression in III. Add that to "sharp" pain and a 33 year old, and it is easy to convince yourself that this is, indeed, pericarditis. This is a good sign for myocardial infarction and does not happen in pericarditis.
Clinician and EKG machine read of acute pericarditis. While it is true that inferior MI has ST depression in aVL 99% of the time (Bischof and Smith), and that inferolateral ST elevation is the most common distribution for pericarditis, the ST elevation in V3 has "terminal QRS distortion (TQRSD)," (diagnostic of LAD occlusion).
This is a value typical for a large subacute MI, n ormal value 48 hours after myocardial infarction is associated with Post-Infarction Regional Pericarditis ( PIRP ). As already mentioned, this patient could have post-infarction regional pericarditis from a large completed MI. Sinus tachycardia has many potential causes. Hammill SC.
It is easy to say pericarditis in such a case. young male no risk factors and ST-elevation in several leads) As Dr. Smith has emphasized many times you diagnose pericarditis at your patient's and your own peril. Version 1 was not trained to detect myo- or pericarditis. The above ECG was recorded. How did the Queen do?
The ECG did not meet STEMI criteria, and the final cardiology interpretation was “ST and T wave abnormality, consider anterior ischemia”. Hence the first ECG was labeled 'anterior ischemia' based on ST depression, rather than identifying this as reciprocal from posterior OMI. But are there any other signs of Occlusion MI? Meyers et al.
In any case, the ECG is diagnostic of severe ischemia and probably OMI. These latter findings are typical of pericarditis, but pericarditis never has reciprocal ST depression. Nossen Comment/Interpretation: Evaluation of ischemia on an ECG can be very challenging. Concordant STE of 1 mm in just one lead or 2a.
This rules out pericarditis, which essentially never has reciprocal ST depression. When flow is restored, wall motion may completely recover so that echocardiogram does not detect the previous ischemia. This is not pericarditis because: a. Pericarditis does not have reciprocal depression.
There is also STE in lead III with reciprocal depression in aVL and I, as well as some subendocardial ischemia pattern with STD in V5-V6 and STE in aVR. Aslanger's is a combination of acute inferior OMI plus subendocardial ischemia, and due to the ischemia vectors , it has STE only in lead III. Moreover, there is tachycardia.
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. The ECG does not show any signs of ischemia. True Positive ECG#2 : Also sinus rhythm. There is ST depression in V1.
Alternation in ST segment appearance ( or in the amount of ST elevation or depression ) — is often linked to ischemia. Repolarization Alternans — entails beat-to-beat variation in the ST segment and/or T wave. Conduction and Refractoriness Alternans — entails variance of impulse propagation along some par t of the conduction system.
Echo does not necessarily differentiate acute MI from pericarditis: both may have wall motion abnormalities. The septum appears a bit darker than the rest, and you might be fooled into thinking there is ongoing ischemia here. See an examples of CT ischemia here. There was a CT chest image from the previous day.
Haven't you been taught that this favors pericarditis? Weren't you taught that concave morphology favors pericarditis? Weren't you taught that "new tall T wave in V1" is concerning for ischemia, and so this is the opposite? Expert ECG interpretation can often distinguish normal variant STE from OMI from pericarditis.
More Smith comment: it is true that ST depression (STD) due to subendocardial ischemia does not localize [it is usually diffuse ST depression, in multiple leads and not reciprocal to ST elevation in an opposite territory], this ST depression is different! Notice how useful serial ECGs are! mm ST depression in aVL. mm ST depression in aVL.
More likely, the patient had crescendo angina, with REVERSIBLE ischemia for 48 hours that only became potentially irreversible (STEMI) at that point in time. During the 48 hours of angina, such reversible ischemia often leads to myocardial stunning with akinesis of the myocardial wall that puts it at risk for thrombus. Re-occlusion 2.
The ECG shows sinus tachycardia with RBBB and LAFB, without clear additional superimposed signs of ischemia. ECG of pneumopericardium and probable myocardial contusion shows typical pericarditis Male in 30's, 2 days after Motor Vehicle Collsion, complains of Chest Pain and Dyspnea Head On Motor Vehicle Collision. ST depression.
The differential is: Posterolateral OMI or subendocardial ischemia The distinction between posterior OMI and subendocardial ischemia can be important and sometimes difficult. Ischemic ST depression includes posterior OMI and subendocardial ischemia. Her prior ECG on file is shown below: What are your next steps?
Normal RBBB, no evidence of ischemia. Patients with completed, transmural infarct are also at risk for post-infarction regional pericarditis and myocardial rupture. In figure 3, I have inverted the image vertically to simulate recording leads from the opposite polarity (see Figure 3 ). R-waves of of normal height.
Well, don't we see diffuse ST Elevation in Myo-pericarditis (with STD in aVR)? Our chief of cardiology, Gautam Shroff, interprets it differently and thinks this is indeed ischemia. So this is STEMI, right? Which artery? There is ST Elevation in every lead except aVR (STD in aVR). Could this be myopericarditis?
Pericarditis is rare — but myocarditis is not , so especially in this age group — more information is needed to quickly determine if this could be an acute MI, myocarditis, or none of the above.
In terms of ischemia, there is both a signal of subendocardial ischemia (STD max in V5-V6 with reciprocal STE in aVR) AND a signal of transmural infarction of the inferior wall with Q wave and STE in lead III with reciprocal STD in I and aVL. The rhythm is atrial fibrillation. The QRS complex is within normal limits. These include.
They include myocardial ischemia, acute pericarditis, pulmonary embolism, external compression due to mass over the right ventricular outflow tract region, and metabolic disorders like hyper or hypokalemia and hypercalcemia.
Pericarditis? For coronary anatomy, see here: [link] This is the post intervention ECG: All ST Elevation is gone (more proof that it was all a result of ischemia) Formal Echo: Normal estimated left ventricular ejection fraction - 55%. More likely, these T waves probably reflect ischemia of uncertain age. Is it normal variant?
The second most common cause of medical cardiac tamponade is acute idiopathic pericarditis. Less common etiologies include uremia, bacterial or tubercular pericarditis, chronic idiopathic pericarditis, hemorrhage, and other causes such as autoimmune diseases, radiation, myxedema, etc.
You do NOT see this in normal variant STE, nor in pericarditis. The only time you see this without ischemia is when there is an abnormal QRS, such as LVH, LBBB, LV aneurysm (old MI with persistent STE) or WPW." Here is the patient's troponin I profile: These were interpreted as due to demand ischemia, or type II MI.
Occurrence of “J Waves” in 12-Lead ECG as a Marker of Acute Ischemia and Their Cellular Basis. Prominent J waves and ventricular fibrillation caused by myocarditis and pericarditis after BNT162b2 mRNA COVID-19 vaccination. Occurrence of "J waves" in 12-lead ECG as a marker of acute ischemia and their cellular basis.
2 days later This is a typical LVH pattern, without ischemia Patient underwent 4 vessel CABG. Assessment:" " Nonspecific ST elevation from V1-V4 , question of early repolarization versus pericarditis , question of acute current of injury and ? Pericarditis would be even more unlikely in someone without chest pain.
ECG of pneumopericardium and probable myocardial contusion shows typical pericarditis Male in 30's, 2 days after Motor Vehicle Collsion, complains of Chest Pain and Dyspnea Head On Motor Vehicle Collision. ST depression. Myocardial Contusion?
Pericarditis? These include coronary artery spasm ( as may occur from cocaine use or binge alcohol drinking ) — myocardial bridging ( that may be the cause of intermittent acute ischemia ) — aberrant anatomy of a coronary artery ( which may present with sudden rupture causing acute infarction or sudden death at any age! ).
The patient might be having cardiac ischemia, but if he is, it is unstable angina or non-STEMI, or perhaps he has not YET pseudonormalized, so serial ECGs may be important. Differential of peri-infarct pericardial fluid The differential includes 1) pericarditis with effusion or 2) hemopericardium. Myocardial rupture is not uncommon.
However, with widespread ST depression, this could also be due to diffuse subendocardial ischemia. Everything is complicated by the arrest and hypotension: Is the ischemia caused by the instability, or the instability caused by the ischemia? Myocardial rupture is usually preceded by postinfarction regional pericarditis (PIRP).
Doesn't this necessarily mean that he was having ischemia? These ER patients do not have ischemia and the variation in ST elevation has not been shown to be related to either heart rate or QRS amplitudes ( Variation in ST-Segment Elevation in Early Repolarization: Electrocardiography 40:10,2007 ). She is very good.
Dyspnea, Chest pain, Tachypneic, Ill appearing: Bedside Cardiac Echo gives the Diagnosis 31 Year Old Male with RUQ Pain and a History of Pericarditis. Submitted by a Med Student, with Great Commentary on Bias! Chest pain, SOB, Precordial T-wave inversions, and positive troponin. What is the Diagnosis?
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