This site uses cookies to improve your experience. To help us insure we adhere to various privacy regulations, please select your country/region of residence. If you do not select a country, we will assume you are from the United States. Select your Cookie Settings or view our Privacy Policy and Terms of Use.
Cookie Settings
Cookies and similar technologies are used on this website for proper function of the website, for tracking performance analytics and for marketing purposes. We and some of our third-party providers may use cookie data for various purposes. Please review the cookie settings below and choose your preference.
Used for the proper function of the website
Used for monitoring website traffic and interactions
Cookie Settings
Cookies and similar technologies are used on this website for proper function of the website, for tracking performance analytics and for marketing purposes. We and some of our third-party providers may use cookie data for various purposes. Please review the cookie settings below and choose your preference.
Strictly Necessary: Used for the proper function of the website
Performance/Analytics: Used for monitoring website traffic and interactions
It's a very "fun" ECG, with initial ectopic atrial tachycardia (negative P waves in inferior leads conducting 1:1 with the QRSs), followed by spontaneous resolution to sinus rhythm. In the available view of the sinus rhythm, we see normal variant STE which probably meets STEMI criteria in V4 and V5. Triage ECG: What do you think?
The conventional machine algorithm interpreted this ECG as STEMI. It shows sinus tachycardia with right bundle branch block. Taking a step back , remember that sinus tachycardia is less commonly seen in OMI (except in cases of impending cardiogenic shock). When EMS found her, she was dyspneic and diaphoretic. Both were wrong.
Sinus tachycardia has many potential causes. This is especially true for the elderly patient with sinus tachycardia. What is the cause of the sudden tachycardia? It has been estimated that in the aggregate, they occur at a rate of about 3 per 1000 patients with acute MI, and most of these events occur in patients with STEMI.
This certainly looks like an anterior STEMI (proximal LAD occlusion), with STE and hyperacute T-waves (HATW) in V2-V6 and I and aVL. How do you explain the anterior STEMI(+)OMI immediately after ROSC evolving into posterior OMI 30 minutes later? This caused a type 2 anterior STEMI. The April 8, 2022 post by Drs.
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.
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.
She was diagnosed with a Non-STEMI and kept overnight for a next day angiogram. Medics recorded the above ECG and called a STEMI alert. Her symptoms at the time ECG #1 was obtained were CP and SOB — yet interpretation of this initial tracing prompted a STEMI alert. Her troponin I returned at 900 ng/L.
This point is particularly relevant regarding ECG #2 — because sinus tachycardia is seen on this earlier ECG. In the October 15, 2022 post of Dr. Smith's ECG Blog — Drs. Smith and Meyers in their October 15, 2022 post on Precordial Swirl. What is P recordial S wirl ? NOTE: It's EASY to get fooled by LVH!
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?
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.
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? aVR ST Segment Elevation: Acute STEMI or Not?
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).
The Queen of Hearts correctly says: Smith : Why is this ECG which manifests so much ST Elevation NOT a STEMI (even if it were a 60 year old with chest pain)? In addition to sinus tachycardia, the only abnormalities listed by the computer were "low voltage, precordial leads" and "anteroseptal infarct, old.Q Physician: "No STEMI."
See many examples of Pseudo STEMI due to hyperkalemia at these two posts: Acute respiratory distress: Correct interpretation of the initial and serial ECG findings, with aggressive management, might have saved his life. But the rate is ~130/minute — which is a bit fast for sinus tachycardia. The patient was treated.
22:25 — What if you have a regular SVT ( = narrow-complex tachycardia ) without obvious P waves? ( 2:25 — Dr. Grauer: The 1st Error : Too many clinicians in 2024 are still stuck in the outdated millimeter-based STEMI Paradigm”. ). 19:50 — Not appreciating statistical odds! ( The 4 common causes? — The most commonly overlooked cause? )
If you use quantitative end-tidal CO2 monitoring, there is never any need to waste time making sure that the endotracheal tube is correctly placed. == MY Comment, by K EN G RAUER, MD ( 10/10/2022 ): == Today’s case is a “Save”! Tachycardia is of course, quite common in patients following cardiac arrest.
Later, she developed chest pain again, and had this ECG recorded: Obvious Anterior OMI that is also a STEMI Coronary angiogram- --Right dominant coronary artery system --The left main artery was normal in appearance and free of obstructive disease. --The Thus, Wellens' syndrome should be thought of as a transient OMI or transient STEMI.
Despite the clinical context, Cardiology was consulted due to concerns for a "STEMI". After initiating treatment for hyperkalemia, repeat ECG showed resolution of Brugada pattern: The ECG shows sinus tachycardia. A Very Wide Complex Tachycardia. The April 17, 2022 post ( Leads V1,V2 placed too high ). What is the Rhythm?
T-wave inversions and dynamic ST elevation Tachycardia, hyperthyroid, and ST elevation. Anterior STEMI? Please see My Comment at the bottom of the page in the April 17, 2022 post of Dr. Smith's Blog — for concise review on how to quickly recognize too-high placement of the lead V1 and V2 electrodes. What is it?
Diagnosis: Acute non-ST segment elevation MI (Non-STEMI, or NSTEMI) Second troponin returned at around 0200: 15,894 ng/L 0245 (unclear if ongoing pain or not) Inferoposterior (and lateral V5-6) reperfusion findings. There is sinus tachycardia at 100-105/minute. Admitted to the hospital service for further evaluation and management."
ECG met STEMI criteria and was labeled STEMI by computer interpretation. J waves can also be induced by Occlusion MI (5), STEMI mimics including takotsubo and myocarditis complicated by ventricular arrhythmias (6, 7), and subarachnoid hemorrhage with VF (8). Take home : Not all STEs are STEMIs or OMIs. What do you think?
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.
The status of the patients chest pain at this time is unknown : EKG 1, 1300: There is sinus tachycardia and artifact of low and high frequency. However, there is also significant tachycardia , with heart rate of 116, and known hypoxia. Supply-demand mismatch can cause ST Elevation (Type 2 STEMI). An EKG was immediately recorded.
Ventricular tachycardia?) Learning points: 40% of LAD OMI with TIMI-0 flow do NOT meet STEMI criteria (manuscript under consideration at Eur Ht. 20/53 did not meet STEMI criteria, but all showed OMI diagnosed by both Smith and the Queen of Hearts. He said it felt like "someone ripped [his] heart out." What do you think?
The fear comes built in with the diagnosis often amplified by young felllows on call (& often times by senior consultants as well) It may appear real, from a clinical angle, but trust, when we deal with the whole gamut of so-called ACS (other than STEMI), there is indeed a benign face in many of them. 2022 Oct;38(10):1521-1524.
This ECG was recorded: It is difficult to appreciate P-waves, but I believe this is sinus tachycardia. It is correct that he did not have chest pain, but we must remember that fully 1/3 of full blown STEMI do not present with chest pain. This is extremely elevated for a type 2 MI and totally consistent with STEMI.
Or, there could be mid-ventricular Takotsubo , in which there is poor function ( and ballooning ) o f the mid-LV, with good function at both the base and the apex and, still other anatomic possibilities ( See the June 24, 2014 post and My Comment in the July 21, 2022 post of Dr. Smith's ECG Blog regarding Takotsubo variant patterns ).
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. If the QRS is prolonged, then the differential includes: 1. Hyperkalemia 2. Other drugs with sodium channel blockade: Tricyclic antidepressants.
We organize all of the trending information in your field so you don't have to. Join thousands of users and stay up to date on the latest articles your peers are reading.
You know about us, now we want to get to know you!
Let's personalize your content
Let's get even more personalized
We recognize your account from another site in our network, please click 'Send Email' below to continue with verifying your account and setting a password.
Let's personalize your content