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See our other countless hyperkalemia cases below: General hyperkalemia cases: A 50s year old man with lightheadedness and bradycardia Patient with Dyspnea. A woman with near-syncope, bradycardia, and hypotension What happens if you do not recognize this ECG instantly? Also: How did this happen? Is this just right bundle branch block?
There’s competing sinus bradycardia and junctional rhythm, with otherwise normal conduction, borderline right axis, normal R wave progression and voltages. While STEMI negative, the ECG is diagnostic of proximal LAD occlusion. Transient STEMI” are often managed like non-STEMI with delayed angiography, which is very risky.
There is STE in III and aVF which does not meet STEMI criteria due to insufficient STE in lead aVF. Resuscitation was initiated and this ECG was obtained: Likely AFib (irregularly irregular) with bradycardia. The cardiologists were not familiar with this and insisted that the ECG in paced rhythm could not be used to "look for a 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?
This ECG was read as “No STEMI” with no prior available for comparison. It is true this ECG does not meet STEMI criteria (there is 1.0 Soon afterward, the patient’s symptoms return along with lightheadedness, bradycardia, and hypotension. The Queen of Hearts sees it of course: Still none of these three ECGs meet STEMI criteria.
His first electrocardiogram ( ECG) is given below: --Sinus bradycardia. Take home messages: 1- In STEMI/NSTEMI paradigm you search for STE on ECG. If this patient was managed according to the STEMI/NSTEMI paradigm (although he would be a candidate for early invasive treatment), he would probably be taken to the cath lab hours later.
I will leave more detailed rhythm discussion to the illustrious Dr. Ken Grauer below, but this use of calipers shows that the rhythm interpretation is: Sinus bradycardia with a competing (most likely junctional) rhythm. For national registry purposes, this will be incorrectly classified as a STEMI.) Large STEMI are approximately 30-80.
Here is his ED ECG: There is obvious infero-posterior STEMI. What are you worried about in addition to his STEMI? There is also bradycardia. Bradycardia puts patients at risk for "pause-dependent" Torsades de Pointes. Bradycardia puts patients at risk for "pause-dependent" Torsades de Pointes. Learning Points: 1.
Looking first at the long-lead II rhythm strip — there is significant bradycardia , with a heart R ate just under 40/minute. But the point to emphasize — is that it should only take seconds to recognize that there is bradycardia from significant AV block. = Would you approve her for a nonemergent surgical procedure?
I see the following: The rhythm is sinus bradycardia at ~55-60/minute. These tall T waves are associated with flattening ( straightening ) of the ST segment in the inferior leads — with slight S T elevation in leads V2-thru-V6 ( albeit not enough to qualify as a "STEMI" — Akbar et al, StatPearls, 2023 ).
The ECG shows obvious STEMI(+) OMI due to probable proximal LAD occlusion. There was no evidence bradycardia leading up to the runs of PMVT ( as tends to occur with Torsades ). With longterm use there may be — bradycardia, AV conduction defects and risk of Torsades de Pointes ( especially in patients also on Digoxin ).
I did not think that the T-waves in V2 and V3 are hyperacute and I still do not--I disagree with Ken below--I think they are normal , especially in the context of bradycardia. Their apparently excessive length (QT interval) is due to bradycardia. They do not have much bulk. A corrected QT would be 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.
He reports that this chest pain feels different than prior chest pain when he had his STEMI/OMI, but is unable to further describe chest pain. Sensitivity was 87% for OMI in our validation study (it was 34% for STEMI criteria). MY Thoughts on the ECG in Figure-1: The rhythm in ECG #1 is sinus bradycardia at ~50-55/minute.
The Initial ECG in Today's Case: ECG #1 showed sinus bradycardia at a rate slightly under 60/minute — normal intervals — slight left axis ( about -15 degrees ) — and no chamber enlargement. Figure-1: I've labeled the 1st, 2nd and 4th tracings in today's case ( See text ).
Here is his ED ECG: There is bradycardia with a junctional escape. There is an obvious inferior posterior STEMI(+) OMI. Case continued A bedside ultrasound showed diminished LV EF and of course bradycardia. Results Of 149 patients with inferior STEMI , 43 (29%) had RVMI and 106 (71%) did not. What is the atrial activity?
Sinus bradycardia, normal conduction, normal axis, normal R wave progression, no hypertrophy. Step 1 to missing posterior MI is relying on the STEMI criteria. A prospective validation of STEMI criteria based on the first ED ECG found it was only 21% sensitive for Occlusion MI, and disproportionately missed inferoposterior OMI.[1]
The receiving emergency physician consulted with interventional cardiology who stated there was no STEMI. Is there STEMI? About one hour later his high sensitivity troponin I resulted at 3,000 ng/L (reference 3-54 ng/L). The patient continued having chest pain. Fortunately the patient was then taken for angiography. Do not treat AIVR.
The provider contacted cardiology to discuss the case, but cardiology "didn't think it was a STEMI, didn't think he needed emergent cath." JAMA 2000) showed that 1/3 of patients with STEMI, and 1/3 of patients with NSTEMI, present without chest pain. The whole paradigm is literally called "STEMI" vs. "NSTEMI." Canto et al.
While undergoing a stress test as a part of the non-invasive approach, she developed chest pain and hypotension and had this ECG: There is sinus bradycardia with massive inferior ST elevation, as well as ST elevation in V1-V3, diagnostic of inferior and right ventricular (RV) STEMI.
In any case, there is bradycardia. Although most cardiac arrest from MI is due to ventricular fibrillation, some is due to high grade AV block, and so this could indeed be due to large acute STEMI. LV anterior STEMI does not give maximal ST elevation in V1. So this ECG is typical of right ventricular (RV) STEMI.
The emergency physician asked the advice of Dr. Reiters because of absence of STEMI criteria. The app also states that there is "suspected" ACS without ST elevation (NSTEMI), posterior fascicular block, sinus bradycardia, and LVH) Note on version 1 of the Queen: she will diagnose "OMI" whether it is an active or reperfused OMI.
Three months prior to this presentation, he received a pacemaker for severe bradycardia and syncope due to sinus node dysfunction. His EKG with worse pain now shows enough ST elevation to meet STEMI criteria. The EKG was read by the conventional computer algorithm as diagnostic of “ACUTE MI/STEMI”.
Later, I found old ECGs: 5 month prior in clinic: V5 and V6 look like OMI 9 months prior in clinic with no chest symptoms: V5 and V6 look like OMI 1 year prior in the ED with chest pain: V5 and V6 sure look like a STEMI For this ECG and chest pain in the ED, the Cath lab activated. But the angiogram was clean. There was no OMI.
If it is STEMI, it would have to be RBBB with STEMI. Bradycardia. But — one of the causes of Brugada Phenocopy is acute infarction — so I didn’t know how to distinguish between a preexisting Brugada-1 ECG pattern vs a Brugada ECG pattern developing as a result of acute ongoing anterior STEMI. Is it Brugada pattern?
Despite the clinical context, Cardiology was consulted due to concerns for a "STEMI". Hyperkalemia causes peaked T waves and the "killer B's of hyperkalemia", including bradycardia, broad QRS complexes, blocks of the AV node and bundle branches, Brugada morphology, and otherwise bizarre morphology including sine wave. With a twist.
It doesn’t meet any conventional STEMI criteria, but there is patently obvious increased area under the curve. But until its magic is available at bedside the clinician must train his/her eyes to spot the subtle features of OMI, and equally allow the bias of STEMI to fossilize. Is this OMI?
These kinds of cases were excluded from the study as obvious anterior STEMI. --QTc Case 1 Acute anterior STEMI from LAD occlusion, or Benign Early Repolarization (BER)? Appropriately, the physicians repeated the ECG 20 minutes later and it was diagnostic of anterior STEMI. Why bradycardia? QTc is the computer measurement.
We have borderline sinus bradycardia with 1 ° AVB and occasional PACs. ECG diagnosis: Borderline sinus bradycardia, 1st degree AVB, RBBB, and occasional PACs. Generally speaking, right bundle branch block does not mimic, or obscure, the ECG diagnosis of acute STEMI the way left bundle branch block does. What’s the rhythm?
Repeat ECG showing no STEMI, only non-specific ST-segment and T-wave abnormalities, unchanged from prior" Transferred to surgery for exploration but diagnostic studies were too indeterminate to be certain of intra-abdominal pathology. Trop T now very high, well into the range one sees with a STEMI; very unusual in type II MI.
Here is his previous ECG: This was my interpretation of the first ECG: Sinus bradycardia with less than 1mm ST elevation in V4-V6, elevated compared to the previous ECG, suggestive of lateral MI. Moreover, T-wave inversion in aVL was also found to be 100% sensitive and 86% specific for inferior STEMI. mm ST depression in aVL.
Is it STEMI? Syncope and Bradycardia Syncope in a 20-something woman Long QT: Do not trust the computerized QT interval when the QT is long An Alcoholic Patient with Syncope Cardiac Arrest. Chest pain in high risk patient. Are these Hyperacute T-waves? What is going on here?
Any objective, rule-based analysis of this ECG would scream "STEMI" or "OMI". And I recognized this as a STEMI mimic. Instead — my thoughts were as follows: The rhythm is sinus , with marked bradycardia and a component of sinus arrhythmia. There are Q-waves in V4-V6, with what appear to be hyperacute T-waves.
The computer interpreted the ECG (GE Marquette 12 SL) as: "Sinus Bradycardia. Here it is: Computer interpretation: "Sinus bradycardia. This was sent to me by a former resident from a community hospital: A middle-aged woman complained of chest pain and was seen in triage. She had a ECG recorded. Normal ECG."
A prehospital ECG was recorded (not shown and not seen by me) which was worrisome for STEMI. A previous ECG from 4 years prior was normal: This looks like an anterior STEMI, but it is complicated by tachycardia (which can greatly elevate ST segments) and by the presentation which is of fever and sepsis.
The ECG shows sinus bradycardia but is otherwise normal. Written by Willy Frick A 46 year old man with a history of type 2 diabetes mellitus presented to urgent care with complaint of "chest burning." The documentation does not describe any additional details of the history. The following ECG was obtained. ECG 1 What do you think?
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. .: See these 3 other posts of sinoventricular rhythm The K came back at 6.2 The patient was treated.
There is sinus bradycardia with one PVC. This is a troponin I level that is almost exclusively seen in STEMI. So this is either a case of MINOCA, or a case of Type II STEMI. If the arrest had another etiology (such as old scar), and the ST elevation is due to severe shock, then it is a type II STEMI.
Whatever today's rhythm turns out to be — the "good news" is that the bradycardia and degree of AV block is likely to improve as soon as there is reperfusion of the "culprit" artery ( Therefore need for prompt cath with PCI ). ECG Blog #218 — Reviews HOW to define a T wave as being H yperacute ?
Without seeing the patient, my interpretation of the first ECG was: likely normal variant ST-elevation (early repolarization), with a small possibility of pericarditis, and almost no possibility of acute coronary occlusion (STEMI). and therefore highly unlikely to be STEMI.
After the heart rate increased slightly, here was the repeat ECG: Sinus bradycardia, only slightly faster rate than prior. Learning Points: Ectopic atrial rhythm can produce atrial repolarization findings that can be confused for acute ischemia, STEMI, or OMI.
But it doesn’t meet STEMI criteria, and was not identified by the computer or the over-reading cardiologist. Still no WPW pattern, and more obvious inferoposterior OMI, but still STEMI negative. The emergency physician wasn’t sure what to make of the changes from one ECG to the next but was concerned about ACS. What do you think?
My Thoughts on the Initial ECG: Systematic interpretation of ECG #1 shows: Sinus bradycardia at ~55-60/minute — normal intervals ( PR-QRS-QTc ) — normal frontal plane axis ( about +20 degrees ) — no chamber enlargement. At this point — I learned a bit more about today's patient: The patient is a man who had an inferior STEMI in 2010.
It does not meet STEMI criteria. Obvious STEMI(+) OMI of inferior, posterior, and lateral walls, now with likely 2nd degree heart block type 1 (Wenckebach). Learning Points: We can find OMI on ECG much sooner than STEMI criteria in many cases, and of course many OMIs never meet STEMI criteria at all. Easy for anyone.
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