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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. ( Some residual ischemia in the infarct border might still be present. Both episodes are initiated by an "R-on-T" phenomenon.
The first task when assessing a wide complex QRS for ischemia is to identify the end of the QRS. The ST segment changes are compatible with severe subendocardial ischemia which can be caused by type I MI from ACS or potentially from type II MI (non-obstructive coronary artery disease with supply/demand mismatch). What do you think?
Discontinue all negative chronotropic agents, since the risk of torsade is much higher with bradycardia or pauses. It should be kept in mind that on occasions, beta-one agonist can result in increased ventricular ectopy e.g., in severe myocardial ischemia (by increasing myocardial demand), or sometimes with congenital long-QT syndrome.
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." QUESTION #2: If it were not for the markedly prolonged QTc — Wouldn't ECG #1 look like diffuse subendocardial ischemia?
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.
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. Ischemia/infarction. Bradycardia. Hypothermia.
See this case, where a patient with BTWI morphology and dramatic EKG changes within minutes is diagnosed with myocarditis: [link] com/2019/07/what-does-this- ecg-with-significant-st.html EKG 3 also has a saddleback morphology in V2, which is only rarely due to OMI. Still, such dramatic changes cannot be overlooked.
But when the clinical presentation is sepsis, one must entertain the possibility that the ST elevation is due to demand ischemia, or some other process, and exacerbated by tachycardia. It is prudent to treat the other conditions, get the heart rate controlled, and repeat the ECG.
The patient later settled into sinus bradycardia. He was started on amiodarone and had no more events. Next day, the cardiologists were convinced (I think correctly) that this was SVT with aberrancy that was triggered by DKA.
Altered Mental Status, Bradycardia == MY Comment , by K EN G RAUER, MD ( 2/2 /2024 ): == Dr. Meyers began today’s case with the clinical challenge of asking you to identify the underlying cause of ECG #2. -- Read this ECG -- Osborn Waves and Hypothermia (this is the "Figure" above) What does LBBB look like in severe hypothermia?
Both of these features make inferior + RV MI by far the most likely ( Pseudoanteroseptal MI is another name for this ) There is also sinus bradycardia and t he patient is in shock with hypotension. A narrow complex bradycardia without any P-waves is also likely to respond to atropine, as it may be a junctional rhythm.
IF the Patient is Younger and Athletic: The mechanism of AFib in younger, athletic individuals is often heavily influenced by increased vagal tone ( Rao and Shipon — ACC, 2019 — and — Calvo et al — Br J Sports Med, 2012 ). Baseline bradycardia in endurance athletes limits the use of ß-blockers.
No more abnormal U-waves == MY Comment, by K EN G RAUER, MD ( 11/18/2019 ): == LOTS of great points regarding use of the ECG in association with electrolyte abnormalities. U waves may also be found in patients with LVH and/or bradycardia , or occasionally as a normal variant. N OTE # 1 — U waves are not specific for hypokalemia!
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.
For coronary anatomy, see here: [link] This is the post intervention ECG: All ST Elevation is gone (more proof that it was all a result of ischemia) Formal Echo: Normal estimated left ventricular ejection fraction - 55%. This is sinus bradycardia. More likely, these T waves probably reflect ischemia of uncertain age.
Heart Rhythm, 15(10), e73-e189. -- Comment by K EN G RAUER, MD ( 1/30/2019 ): -- Superb presentation and discussion by Dr. Alexandra Schick ( with edits by Dr. Smith ) of an elderly woman who was seen in the ED for altered mental status, hyperthermia, and the initial ECG shown above. Heart Rhythm, 15(9): 1394-1401. [7]
These include ( among others ) — acute febrile illness — variations in autonomic tone — hypothermia — ischemia-infarction — malignant arrhythmias — cardiac arrest — and especially Hyperkalemia. Other Arrhythmias ( PACs, PVCs, AFib, Bradycardia and AV conduction disorders — potentially lethal VT/VFib ).
Osborn waves have been reported with hypercalcemia, brain injury, subarachnoid hemorrhage, Brugada syndrome, cardiac arrest from VFib — and — severe, acute ischemia resulting in acute MI ( See My Comment in the November 22, 2019 post on Dr. Smith’s Blog ). Rituparna et al — as well as Chauhan and Brahma ( Int.
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