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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.
A small proportion of patients with STEMI treated via primary PCI experienced late ventricular tachycardia (VT) or ventricular fibrillation (VF), occurring one or more days following the procedure, but late VT or VF with cardiac arrest occurred rarely, especially among patients with uncomplicated STEMI, according to a study published in JAMA Network (..)
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??
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?
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.
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.
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.
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?
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.
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.
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.
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.
KEY Point: Look for additional simultaneously-recorded leads = “12 Leads are Better than One!” ( ie, For example with tachycardias — the QRS may look narrow if all you have is 1 or 2 leads — whereas if part of the QRS lies on the baseline in the single lead you are looking at, this might be VT! ). 19:50 — Not appreciating statistical odds! (
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.
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.
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.
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.
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.
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.
Background Early ventricular tachycardia/fibrillation (VT/VF) in patients with ST-elevation myocardial infarction (STEMI) has higher morbidity and mortality. This study examines gender-differentiated risk factors and underlying mechanisms for early onset VT/VF in STEMI. vs. 61.0 ± 13.0 vs. n = 46, L5: 4.3 ± 9.9%, P = 0.016).
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.
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.
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?
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?
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. Junctional tachycardia? ).
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.
Is this an anterior STEMI with LBBB? Explanation : The patient had a worrisome history: 59 yo with significant substernal chest pressure, so his pretest probability of MI (and even of STEMI) is reasonably high. Additionally, appropriate discordance is common in NonSTEMI, but very unusual in coronary occlusion (STEMI).
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?
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).
There is sinus tachycardia. Sinus tachycardia, which exaggerates ST segments and implies that there is another pathology. I have always said that tachycardia should argue against acute MI unless there is cardiogenic shock or 2 simultaneous pathologies. Here is that ECG: What do you think? See Table for diagnostic utility.
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. The rhythm looks fairly regular — and atrial activity is absent. What is S hark F in M orphology ?
The "criteria" for posterior STEMI are 0.5 Is it STEMI or NonSTEMI? The patient had no hypertension, no tachycardia, a normal hemoglobin, no drug use, no hypotension/shock, no murmur of aortic stenosis. The troponin I returned at 4.1 ng/mL (ULN = 0.030 ng/mL) , diagnostic of myocardial injury. mm STE in one lead.
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?
There is sinus tachycardia. The possibility of anterior STEMI was not noticed during patient care. I saw this as I was reading a large a stack of ECGs: What do you think? The T-waves are slightly peaked, suggesting hyperkalemia. But what is atypical is that the T-wave in V3 towers over the R-wave. The QTc is 462 ms. It was stented.
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 ”. The patient received a diagnosis of “NSTEMI” and angiography was scheduled for the next day.
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. BOTTOM Line: The ECG in Figure-4 shows an extensive infero-postero-lateral STEMI.
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!!
If this was a tachycardia at a rate of 150, it might appear to be a narrow complex tachycardia, when in fact, it would be a wide complex tachycardia! Generally speaking, right bundle branch block does not mimic, or obscure, the ECG diagnosis of acute STEMI the way left bundle branch block does. An ECG is captured.
In other words, after reperfusion therapy for STEMI, the appearance of AIVR is usually a good sign, meaning that the artery is reperfused. Our electrophysiologist, Rehan Karim, states he has ablated AVNR"T" ("T" because it is not tachycardia) in a 90 year old, and that he has seen rate-related BBB at very slow rates.
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.
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."
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