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Below is the first ECG recorded by paramedics after 2 hours of chest pain, interpreted by the machine as “possible inferior ischemia”. There’s competing sinus bradycardia and junctional rhythm, with otherwise normal conduction, borderline right axis, normal R wave progression and voltages. What do you think?
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. The fact that R waves 2 through 6 are junctional does make ischemia more difficult to interpret -- but not impossible.
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 STD maximal in V1-V4 is diagnostic of acute transmural posterior wall ischemia, most likely due to posterior OMI. Subendocardial ischemia does not localize, and subendocardial ischemia presents with STD maximal in V5-6, II, and STE in aVR. It does not meet STEMI criteria. Subendocardial ischemia does not localize.
The patient with no prior cardiac history presented in the middle of the night with acute chest pain, and had this ECG recorded during active pain: I did not see any ischemia on this electrocardiogram. Their apparently excessive length (QT interval) is due to bradycardia. This is a case I had quite a while back.
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]
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. Whether these EKGs show myocarditis, a normal variant, or something else, they are overall not typical of transmural ischemia of the anterior or high lateral walls.
Here is his ECG: There is no clear evidence of OMI or ischemia. 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. A 40-something male with no previous cardiac disease presented with chest pain.
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.
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.
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. QTc is the computer measurement. 100% LAD occlusion.
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.
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. 2] Conduction through the accessory pathway can be intermittent (with different degrees of pre-excitation), and affected by ischemia.
Here was my answer: "Not ischemia. 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. This was texted to me in real time.
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.
Diffuse ST depression with ST elevation in aVR: Is this pattern specific for global ischemia due to left main coronary artery disease? Ischemia b. ST depression: is it ischemia? In my experience, Ive seen U waves not only with low K+/low Mg++ but also in patients with bradycardia, LVH, and sometimes in normal subjects.
Here are inferior leads, and aVL, magnified: A closer inspection of the inferior leads and aVL Sinus bradycardia. 3) STEMI criteria failed to identify this acute coronary occlusion, like many others. I had no history on the case and no prior ECG for comparison. What do you think?
Triage physician interpretation: -sinus bradycardia -lateral ST depressions While there are lateral ST depressions (V5, V6) the deepest ST depressions are in V4. Ischemic ST-Segment Depression Maximal in V1-V4 (Versus V5-V6) of Any Amplitude Is Specific for Occlusion Myocardial Infarction (Versus Nonocclusive Ischemia). 121.022866.
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?
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.
There’s sinus bradycardia, first degree AV block, normal axis, delayed R wave progression, and normal voltages. There’s minimal concave ST elevation in III which does not meet STEMI criteria, so this ECG is "STEMI negative". Use STEMI criteria to identify acute coronary occlusion: the ECG was STEMI negative 2.
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.
A prior ECG was available for comparison: Normal One might be tempted to interpret the ST depression as ischemia, but as Smith says, "when the QT is impossibly long, think of hypokalemia and a U-wave rather than T-wave." Is it STEMI? Instead — it commonly reflects ischemia from severe underlying coronary disease.
The ECG shows obvious STEMI(+) OMI due to probable proximal LAD occlusion. There is no definite evidence of acute ischemia. (ie, Simply stated — t he patient was having recurrent PMVT without Q Tc prolongation, and without evidence of ongoing transmural ischemia. ( The below ECG was recorded.
The receiving emergency physician consulted with interventional cardiology who stated there was no STEMI. Is there STEMI? Possible mechanisms of ventricular arrhythmias elicited by ischemia followed by reperfusion. About one hour later his high sensitivity troponin I resulted at 3,000 ng/L (reference 3-54 ng/L). Moffat, M.
In any case, there is bradycardia. There is ST depression beyond the end of the wide QRS in I, II, aVF, and V4-V6, diagnostic of with subendocardial ischemia. 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.
If it is STEMI, it would have to be RBBB with STEMI. Followup ECG: No Change Absence of evolution is the best evidence against ischemia as the etiology. I was taught that the tell-tale sign of ischemia vs an electrical abnormality was in the hx, i.e. chest pain for the ischemia and potential syncope for brugada.
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.
2) The STE in V1 and V2 has an R'-wave and downsloping ST segments, very atypical for STEMI. Cardiology was consulted and they agreed that the EKG had an atypical morphology for STEMI and did not activate the cath lab. Smith comment: 1) Brugada ECG may have ST shifts in limb leads as well as precordial leads. Bicarb 20, Lactate 4.2,
Despite the baseline artifact theres sinus bradycardia, convex ST elevation in III, reciprocal ST depression in aVL and possible anterior ST depression indicating inferoposterior OMI. STEMI criteria are only 43% sensitive for OMI. Beware confusing the diagnosis of posterior STEMI by using posterior leads.
A 12-lead was recorded, showing "STEMI," but is unavailable. Moreover, if you know that catastrophic intracranial hemorrhage can result in an ECG that mimics STEMI, then you know that this patient probably has a severe intracranial hemorrhage. She was BVM ventilated and suctioned. Shortly thereafter, pulses were lost.
ECG met STEMI criteria and was labeled STEMI by computer interpretation. This ECG shows a sinus bradycardia with a normal conduction pattern (normal PR, normal QRS, and normal QTc), normal axis, normal R-wave progression, normal voltages. Hypothermia can also produce bradycardia and J waves, with a pseudo-STEMI pattern.
Within ten minutes, she developed bradycardia, hypotension, and ST changes on monitor. Bradycardia and heart block are very common in RCA OMI. It is possible there is microvascular dysfunction producing residual transmural ischemia. He told the patient this horrible news. The other point in favor of RCA is junctional rhythm.
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