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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.
Easy LINKS — tinyurl.com/KG-ECG-Podcasts — [link] — Other ECG Audio PEARLS I previously made for my ECG Blog can be found in the right column of each page on this blog just below this icon — under, "ECG Audio PEARLS". Get a post -conversion 12-lead ECG — and compare this to the initial 12-lead ECG obtained during the tachycardia!
Voltage for LVH is satisfied — at least by Peguero Criteria ( Sum of deepest S in any chest lead + S in V4 ≥23 mm in a woman — as discussed in ECG Blog #73 ). 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.
But for those wanting a "simpler" approach" — Consider the following ( which I review below in my ADDENDUM ): This patient is in a wide, "ugly-looking" and seemingly regular tachycardia without P waves. Regarding Q - R - S - T Changes: There is a Q wave in lead III. R wave progression is not normal.
By the P s, Q s, 3 R Approach ( as reviewed in ECG Blog #185 ): The Q RS complex is obviously wide. Given the rapid rate of the tachycardia and the amorphous shape of the QRS — the decision was made to sedate the patient and cardiovert. ECG Blog #185 — Systematic P s, Q s, 3 R Approach to Rhythm Interpretation.
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?
He was rushed by residents into our critical care room with a diagnosis of STEMI, and they handed me this ECG: There is sinus tachycardia with ST elevation in II, III, and aVF, as well as V4-V6. At first glance, it seems the patient is having a STEMI. Then ACS (STEMI) might be primary; this might be cardiogenic shock.
The finding of a fairly regular, wide tachycardia without clear sign of atrial activity ( especially when seen in an acutely symptomatic patient ) — should immediately prompt a diagnosis of VT until proven otherwise. ECG Blog #265 — Reviews a case of Shark-Fin ST Elevation. What is S hark F in M orphology ?
Cardiac arrest #3: ST depression, Is it STEMI? Confirmation of sinus tachycardia should be easy to verify when the heart rate slows a little bit ( as the patient's condition improves ) — allowing clearer definition between the T and P waves. In this case, the cath lab was activated and the patient had a normal angiogram.
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.
This ECG was texted to me with the implied question "Is this a STEMI?": I responded that it is unlikely to be a STEMI. Septal STEMI often has ST depression in V5, V6, reciprocal to V1. Then combine with clinical presentation and low pretest probability 2 Saddleback STEMIs A Very Subtle LAD Occlusion.T-wave wave in V1??
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.
Here are more examples of wide complex tachycardia: these are all a mix of ventricular tachycardia and SVT with aberrancy. There is tachycardia, and there is a wide complex. This wide complex tachycardia could easily be misdiagnosed as V tach. This 51 yo male complained of chest pain, then had a v fib arrest.
when the usual negative P wave deflection of sinus tachycardia is nowhere to be found in lead V1 )? While of course possible for the rhythm in ECG #1 to be either AFlutter or fascicular VT — sinus tachycardia immediately becomes a much more likely possibility once we know that this patient is critically ill with multisystem disease.
There was concern that the rhythm might represent ventricular tachycardia, so lidocaine was given and one attempt at cardioversion was performed. Peaked T waves: Hyperacute (STEMI) vs. Early Repolarizaton vs. Hyperkalemia What will you do for this altered and bradycardic patient? A Very Wide Complex Tachycardia.
A male in his 40's who had been discharged 6 hours prior after stenting of an inferoposterior STEMI had sudden severe SOB at home 2 hours prior to calling 911. Here is his ED ECG: There is sinus tachycardia. Is this acute STEMI? Is this an acute STEMI? -- Unlikely! He had no chest pain.
So this NSTEMI was likely a STEMI(-)OMI with delayed reperfusion. The patient was admitted as ‘NSTEMI’ which is supposed to represent a non-occlusive MI, but the underlying pathophysiology is analogous to a transient STEMI. See these posts: Chest Pain, ST Elevation, and an Elevated Troponin: Should we Activate the Cath Lab?
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.
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. This prompted cath lab activation.
His previous echo one month prior shows the same thing: “consistent with old infarct in LAD vascular territory, with EF 45%” "I think there is something else causing his tachycardia which is exaggerating his EKG findings and mimicking an acute myocardial infarction." The patient spontaneously converted back to sinus tachycardia.
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?
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.
Only very slight STE which does not meet STEMI criteria at this time. I am immediately worried that this OMI will not be understood, for many reasons including lack of sufficient STE for STEMI criteria, as well as the common misunderstanding of "no reciprocal findings" which is very common with this particular pattern.
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.
Here is his ED ECG: There is obvious infero-posterior STEMI. What are you worried about in addition to his STEMI? Comments: STEMI with hypokalemia, especially with a long QT, puts the patient at very high risk of Torsades or Ventricular fibrillation (see many references, with abstracts, below). There is atrial fibrillation.
At 2111, the troponin I peaked at 12.252 ng/mL (this is in the range of STEMI patients, quite high). The conventional computer algorithm called “ sinus tachycardia, otherwise normal EKG ”. Regular readers of this ECG Blog will be well familiar with many of these points.
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.
Other than tachycardia, Other than slight tachycardia, vitals were within normal limits (including oxygen saturation). The provider contacted cardiology to discuss the case, but cardiology "didn't think it was a STEMI, didn't think he needed emergent cath." The whole paradigm is literally called "STEMI" vs. "NSTEMI."
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.
The cardiologist agreed that the ECG was suggestive of STEMI, but the facility's cath lab was apparently not available and he therefore recommended emergent transfer to a cath capable facility. Due to the chest pain radiating into the patient's back, the ER physician ordered CTA chest to rule out aortic dissection.
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. ECG Findings that Suggest Acute PE: We have presented numerous cases of acute PE in multiple posts in Dr. Smith’s ECG Blog. Her troponin I returned at 900 ng/L.
One might think this represents acute STEMI, or Bundle branch block with discordant ST segments and suspicously concordant T-waves. Upon arrival to the ED, he had the following 12-lead ECG: There is striking ST segment elevation in V1 and V2, with ST depression in V3-V6 as well as I, II, and aVF. There is also a wide QRS.
This is ischemic ST depression, and could be due to increasing tachycardia, with a heart rate over 130, but that is unlikely given that the patient is now complaining of crushing chest pain and that there was tachycardia all along. There is widespread ST depression. Figure-1: Comparison of the first 2 ECGs in today's case.
This has been discussed many times before on this blog. In-depth discussion is beyond the scope of this blog. Automatic activity refers to enhanced pacemaking function (typically from a non sinus node source), for example atrial tachycardia. Is there STEMI? The patient continued having chest pain. What is the rhythm?
for those of you who do not do Emergency Medicine, ECGs are handed to us without any clinical context) The ECG was read simply as "No STEMI." and tachycardia, 1.8. Finally , they found that S1Q3T3, precordial T-wave inversions V1-V4, and tachycardia were independent predictors of PE. inverted T-waves in V1 and V2, 1.8;
This is the ECG of a 50 yo old woman who collapsed, was found to have a pulse, but then found to be in ventricular tachycardia. The cath lab was activated for STEMI, but the patient had clean coronaries. This is highly suspicious for acute anterior STEMI. She was shocked into sinus rhythm. She presented to the ED comatose.
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?
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?
Precordial ST depression may be subendocardial ischemia or posterior STEMI. If you thought it might be a posterior STEMI, then you might have ordered a posterior ECG [change leads V4-V6 around to the back (V7-V9)]. Notice there is tachycardia. So there was 3-vessel disease, but with an acute posterior STEMI.
Is this inferor STEMI? Tachycardia and ST Elevation. Atrial Flutter with Inferior STEMI? Inferolateral ST elevation, vomiting, and elevated troponin The treating team did not identify the flutter waves and they became worried about possible "STEMI" (despite the unusual clinical scenario). Long-term outcome is unknown.
Does the ECG represent STEMI-negative OMI findings? Putting all the findings together; dyspnea, slight tachycardia, delayed R-wave progression, prominent lateral S waves and ST depression maximal where the P waves are largest all point toward pulmonary disease as the cause of the ECG findings. How would you mange this patient?
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?
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?
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?
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