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The ECG does not show any definite signs of ischemia. It is unclear if the patient was pain free at this time. In fact, the ECG was described as normal, and without serial ECGs or prior ECGs for comparison it could be. Initial high sensitivity troponin I returned at 6ng/L (normal 0.20
Her vital signs were within normal limits except for bradycardia at 55 bpm. It is probably sinus bradycardia with very small/depressed P-waves and prolonged PR interval. P EARL # 4 In my opinion, it is not worth wasting time trying to figure out the specific rhythm diagnosis of a bradycardia when there is hyperkalemia.
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?
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?
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?
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.
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. ECG Blog #184 — illustrates the "magical" mirror-image opposite relationship with acute ischemia between lead III and lead aVL ( featured in Audio Pearl #2 in this blog post ). The PR and QRS intervals are both normal. ECG Blog #230 — How to compare serial ECGs.
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. Do you recognize this ECG yet? Right Bundle Branch Block with ST Elevation in V1?
There are 3 etiologies I always think of with bradycardia and AV block: 1. There was no evidence of ischemia. In addition to ruling out rate-slowing medication serum electrolyte disorders and/or ischemia/infarction as potential causes of bradyarrhythmias one should also rule out hypothyroidism + sleep apnea. Hyperkalemia.
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.
If you put the inferior and posterior findings together, it is diagnostic of OMI This was read as "inferior ischemia" without any other information by Dr. Richard Gray and as probable reperfused inferior-posterior OMI much later by both me and Pendell Meyers, also without any clinical information.
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.
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.
Extensive conduction system abnormalities can have various causes (ischemia, genetic, infectious, amyloid, etc). For example — bradycardia and AV conduction disturbances are not uncommon with Hyperkalemia , with these conduction disturbances most often resolving once serum K+ is corrected.
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. He had multiple episodes of bradycardia and nonsustained ventricular tachycardia. The patient had none of these conditions. Patient 1 remained in the hospital overnight.
Such findings would normally suggest primary ischemia with concomitant surveillance of coronary occlusion, but these ST/T changes might very well be secondary to the Escape mechanism at hand. Lead V2 shows RR’ QRS configuration, and although ST depression is otherwise expected here, the discordance is a bit excessive. 5] Isnard, R.
3 of the 4 have similarly bizarre PVCs. == MY Comment by K EN G RAUER, MD ( 4/29/2020 ): == Cardiac Arrest with Bizarre PVCs/Torsades de Pointes: Intriguing case with many interesting features. Acute ischemia? ECG #5 — This is the 4th ECG done on the patient in this case ( obtained ~6 hours after arrival in the ED ).
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.
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.
ADDENDUM ( 10/24/2020 ): In the past, the diagnosis of Brugada Syndrome required not only the presence of a Brugada-1 ECG pattern — but also a history of sudden death, sustained VT, non-vasovagal syncope or a positive family history of sudden death at an early age. Smith on this blog ( Simply search for Brugada Syndrome! ).
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. Internat J Arrhyth 2020 Uesako H, Fukikawa H, Hashimoto S, et al. As per Drs.
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. Still, an ECG was obtained at 0649hrs: (Digitized by PM Cardio) McLaren: The patient has a high pretest probability based on age, risk factors and symptoms.
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