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Prompt cath is therefore advised if the post-ROSC shows an acute STEMI. The rhythm is regular — at a rate just over 100/minute = sinus tachycardia ( ie, the R-R interval is just under 3 large boxes in duration ). Continuing with assessment of ECG #1 in Figure-2: The rhythm is sinus tachycardia at ~110/minute.
Are Some Cardiologists Really Limited by Strict Adherence to STEMI millimeter criteria? This is the response he got: Interventionist: "No STEMI, no cath. After stabilizing the patient and recording more ECGs, he tried again: Interventionalist: "It isn't a STEMI." It is a STEMI equivalent. We don't know how many though.
A prehospital ECG was recorded (not shown and not seen by me) which was worrisome for STEMI. Here was his initial ED ECG: There is sinus tachycardia at a rate of about 140 There is profound ST Elevation across all precordial leads, as well as I and aVL. A near 60 year old male called 911 for increasingly severe fever and SOB.
The prehospital and ED computer interpretation was inferior STEMI: There’s normal sinus rhythm, first degree AV block and RBBB, normal axis and normal voltages. The paramedic notes called STEMI into question: “EMS disagree with monitor for STEMI callout. Vitals were normal except for oxygen saturation of 94%. Vitals were normal.
While the initial impression might not immediately suggest ventricular tachycardia (VT), a closer examination raises suspicion. Additionally, the qR morphology, particularly in a patient with right bundle branch block (RBBB) type wide QRS complex tachycardia (WQCT), lends further support for VT. What is the rhythm?
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. The two cases were considered: Patient 1 was recognized by the ED provider and the cardiologist as having resolved “STEMI”. He wrote most of it and I (Smith) edited. It was stented.
Here was the ECG: There is sinus tachycardia. So Shark Fin really is just a dramatic representation of STEMI, and can be in any coronary distribution. So this is STEMI, right? This was sent by a reader. A previously healthy 53 yo woman was transferred to a receiving hospital in cardiogenic shock. and K was normal. Which artery?
It definitely does not fulfill STEMI criteria, and I would argue that it would not lead to cath lab activation in most centers. NOTE #1: Sinus tachycardia is not usually seen in an uncomplicated acute MI. . == Below is the ECG of Patient #2 — as interpreted by the QOH. The ECG is diagnostic of occlusion myocardial infarction (OMI).
This has been termed a “STEMI equivalent” and included in STEMI guidelines, suggesting this patient should receive dual anti-platelets, heparin and immediate cath lab activation–or thrombolysis in centres where cath lab is not available. aVR ST segment elevation: acute STEMI or not? Am J Med 2019, 132(5):622-630.
Sent by Dan Singer MD, written by Meyers, edits by Smith A man in his late 30s presented with acute chest pain and normal vitals except tachycardia at about 115 bpm. Here is the Queen of Heart's interpretation: The cath lab had been activated for concern of STEMI. Here is his triage ECG: What do you think? Do you have a prior?
First, we have a narrow-complex, regular tachycardia, with a rate of about 135-140. This narrows our differential for the rhythm down to sinus tachycardia, paroxysmal supraventricular tachycardia (PSVT, or SVT), and atrial flutter. Is this inferor STEMI? Tachycardia and ST Elevation. Christmas Eve Special Gift!!
He commented: "by every measure, this would be RBBB with inferior and lateral STE appearing to be STEMI," but he also noted that there are several features that appear similar to false positives (like the first case above). There is also much STE in V3-V6, especially V4-V6, that must be considered to be STEMI. Peak troponin was 3.21
Here, I do not see OMI (although the ECG is falsely STEMI positive with just over 1 mm STE in V1 and about 2.5 This is sinus tachycardia (rhythm) with complete heart block (AV node function) with ventricular escape rate just below 30. Never forget that sinus tachycardia is the scariest arrhythmia. What do you think?
C linically — the rhythm we see in the long lead II of ECG #3 behaves similar to MAT, even though there is no tachycardia. Baseline and serial ECGs make you much more likely to identify OMI. CLICK HERE — for my detailed discussion of this subject ). A majority of patients with MAT have longstanding pulmonary disease.
(normal variant, not pericarditis) A Young Man with Sharp Chest pain (normal variant, not pericarditis) 24 yo woman with chest pain: Is this STEMI? That said — I illustrate HOW this RATIO is arrived at in Figure-2 , which I have adapted from the 3/16/2019 post in Life-In-The-Fast-Lane. Pericarditis? P EARL # 2 : These words from Drs.
And more cases, if you want, at this link. == My Comment, by K EN G RAUER, MD ( 3/2/2019 ): == The importance of this case lies in recognition of a number of findings, and the differential diagnoses that these findings should evoke. Biphasic T-waves in a Middle-Aged Male with Vomiting Diabetic Ketoacidosis: is there hypokalemia?
International Journal of Cardiology 2019. T-wave inversions and dynamic ST elevation Tachycardia, hyperthyroid, and ST elevation. Anterior STEMI? A similar profile was found for cTnT: baseline, <3.0 (<3.0–3.8) ng/L; 3 hours, 38.3 ng/L ( P <0.001); and 24 hours, 11.0 (7.2–17.4) ng/L ( P <0.001). Paana et al.
In such cases, it is common for tachycardia to exaggerate the ST Elevation And, in fact, there was no new acute MI at this visit - troponins did not rise again. Computer: MI Here is my interpretation: I did not see any NEW acute MI on this ECG This is more consistent with an old MI with persistent ST elevation.
This paper by Bischof and Smith compared inferior MI to pericarditis and found that of 154 patients with inferior STEMI, 17% of whom had less than 1 mm of STE in any inferior lead, all 154 had at least 0.25 One looks for sinus tachycardia and diffuse low voltage but many conditions produce these nonspecific findings.
The ECG shows obvious STEMI(+) OMI due to probable proximal LAD occlusion. This progressed to electrical storm , with incessant PolyMorphic Ventricular Tachycardia ( PMVT ) and recurrent episodes of Ventricular Fibrillation ( VFib ). The below ECG was recorded. He required multiple defibrillations within a period of a few hours.
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. 12 All STEMI patients had very high cTn typical of STEMI (cTnT > 1.0 Cardiovascular Implications of Fatal Outcomes of Patients With Coronavirus Disease 2019 (COVID-19).
ECG is consistent with severe hypokalemia and/or hypomagnesemia causing prolonged QT (QU) at high risk of Torsades (which is polymorphic ventricular tachycardia in the setting of a long QT interval). Polymorphic Ventricular Tachycardia Long QT Syndrome with Continuously Recurrent Polymorphic VT: Management Cardiac Arrest. Is it STEMI?
There is an obvious inferior STEMI, but what else? Besides the obvious inferior STEMI, there is across the precordial leads also, especially in V1. This STE is diagnostic of Right Ventricular STEMI (RV MI). In fact, the STE is widespread, mimicking an anterior STEMI. EKG is pictured below: What do you think?
The attending crews were concerned for SVT with corresponding ischemic hyperacute T waves (HATW) and subsequently activated STEMI pre-hospital. 2] But there is also Sinus Tachycardia! Then, three minutes later… Crews activated STEMI as she deteriorated into PEA arrest. Closer inspection will show that it is Sinus, after all.
Otherwise vitals after intubation were only notable for tachycardia. An initial EKG was obtained: Computer read: sinus tachycardia, early acute anterior infarct. 2) The STE in V1 and V2 has an R'-wave and downsloping ST segments, very atypical for STEMI. A rectal temperature was obtained which read 107.9 Bicarb 20, Lactate 4.2,
There is sinus tachycardia and also a large R-wave in aVR. Drug toxicity , especially diphenhydramine , which has sodium channel blocking effects, and also anticholinergic effects which may result in sinus tachycardia, hyperthermia, delirium, and dry skin. Annals of Noninvasive Electrocardiology 2019. 8, 2019 ) — ( Jan.
The paramedics diagnosis was "Possible Anterolateral STEMI." More proof that a huge STEMI may have normal or near normal initial troponin. 2 More Interesting ECG Findings: T-QRS-D ( T erminal QRS D istortion ) is seen in lead V2 ( for illustration of T-QRS-D See My Comment in the November 14, 2019 post).
It is a wide complex regular tachycardia at a rate of 120. Is it ventricular tachycardia? I fear that many learners would also not easily recognize where the QRS actually ends, and I fear that some may think that this is ventricular tachycardia due to inability to distinguish QRS from ST segment. The ST Elevation is NOT typical.
Whereas the patient's initial ECG shows sinus rhythm and nonspecific ST-T wave abnormalities just 24 minutes later , there is now profound bradycardia with a junctional escape rhythm ( YELLOW arrows highlighting retrograde P waves ) and obvious findings of an acute inferior STEMI.
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