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The ECG does not show any definite signs of ischemia. This combination is often extremely effective for maintaining good longterm outcome ( Lanza and Shimokawa — Eur Cardiol 18: e38, 2023 ). It is unclear if the patient was pain free at this time. Initial high sensitivity troponin I returned at 6ng/L (normal 0.20
During the night, while on telemetry, the patient became bradycardic, with periods of isorhythmic AV dissociation (nodal escape rhythm alternating with sinus bradycardia), and there were sporadic PVCs. Most such rhythms in the setting of ischemia are VF and will not convert without defibrillation. Acute ischemia?
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.
ECG#1 ECG#2 ECG#3 ECG#4 ECG#5 See outcomes of all 5 below, with the Queen of Hearts AI Bot interpretation. Remember, in diffuse subendocardial ischemia with widespread ST-depression there may b e ST-E in lead s aVR and V1. There are well formed R-waves with good voltage/amplitude which is uncommon for ischemia.
Syncope without prodrome is a significant risk factor for cardiac syncope and poor outcome. during which sinus bradycardia and arrhythmia are seen but not to a degree that produces symptoms. Many patients have a T achy- B rady syndrome in which tachyarrhythmias ( most commonly rapid AFib ) alternate with periods of bradycardia.
The ECG shows sinus tachycardia with RBBB and LAFB, without clear additional superimposed signs of ischemia. Atrial fibrillation is also a predictor of worse outcomes in this case (Alborzi). Other Arrhythmias ( PACs, PVCs, AFib, Bradycardia and AV conduction disorders — potentially lethal VT/VFib ).
Outcome and Analysis: ECG 1 is diagnostic of inferior and right ventricular MI. There is a junctional bradycardia. Furthermore, there are T-wave changes in V2 and V3 which are highly suggestive of ischemia, but difficult to localize: anterior? After midnight (now day 3), she complains of shoulder pain and dyspnea.
Opioids associate with worse outcomes in myocardial infarction , probably because they eliminate the pain signal that informs the clinician of the urgency of revascularization. Possible mechanisms of ventricular arrhythmias elicited by ischemia followed by reperfusion. Do not treat AIVR. In fact, use of antidyrhythimcs (e.g.,
Sinus bradycardia, normal conduction, normal axis, normal R wave progression, no hypertrophy. 2] Here there is no posterior ST elevation, but the anterior ST depression is also less—so it is dynamic, confirming acute ischemia. What do you think? But it is still STEMI negative.
Here is PM Cardio's Queen of Hearts interpretation (AI ECG interpretation trained by Meyers, Smith, and PM Cardio team using thousands of cases and their outcomes): The output number ranges from 0 to 1, with numbers closer to zero meaning likely NOT OMI, and numbers closer to 1 meaning OMI.
Patient presentation is important This was a 60-something with acute chest pain: There is sinus bradycardia at a rate of 44. To me, this makes the ECG nearly diagnostic of ischemia, though if it is LAD occlusion, there should be ST depression in III and aVL, so it is a bit confusing. Why bradycardia? 100% distal LAD occlusion.
There is also bradycardia. Bradycardia puts patients at risk for "pause-dependent" Torsades de Pointes. Torsades in acquired long QT is much more likely in bradycardia because the QT interval following a long pause is longer still. The patient stabilized and had a good outcome. There is atrial fibrillation.
Case outcome The Na was 109. U waves may also be found in patients with LVH and/or bradycardia , or occasionally as a normal variant. This is often quite challenging to recognize — but the finding of negative U waves in a patient with chest pain is highly suggestive of ischemia ! This was the etiology of seizures.
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.
Cardiac Syncope ("True Syncope") Independent Predictors of Adverse Outcomes condensed from multiple studies 1. Evidence of acute ischemia (may be subtle) vii. Thus, if there is documented sinus bradycardia, and no suspicion of high grade AV block, at the time of the syncope, this is very useful. Left BBB vi. LVH or RV d.
There’s sinus bradycardia, first degree AV block, normal axis, delayed R wave progression, and normal voltages. Hyperacute T waves are deflating, suggesting reperfusion but there is still reciprocal change in I/aVL and ST depression in V2, and the bradycardia is worse. Below is the ECG. What do you think? Take home 1. second ).
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. Prevalence and outcome of patients with non-ST segment elevation myocardial infarction with occluded culprit artery - a systemic review and meta-analysis.
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. Was her outcome to be expected for ostial RCA OMI? He told the patient this horrible news.
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