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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?
Even if we stopped here — We could conclude the following: There is marked bradycardia in today's rhythm ( ie, Heart rate in the low 30s ). Finally — If today's patient does not have significant underlying coronary disease — then her bradycardia with AV block may be the result of SSS ( S ick S inus S yndrome ).
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.
The ECG shows sinus tachycardia with RBBB and LAFB, without clear additional superimposed signs of ischemia. Retrieved July 2, 2022, from [link] Moyé, D. Retrieved July 2, 2022, from [link] Sybrandy, K. Other Arrhythmias ( PACs, PVCs, AFib, Bradycardia and AV conduction disorders — potentially lethal VT/VFib ).
It should be treated as such unless there is more information such as old or serial EKGs that can confirm a benign diagnosis, as BTWI patterns can mimic the South Africa Flag Sign (Compare this EKG to case 4 here: [link] com/2022/05/quiz-post-which- of-these-if-any-are-omi.html ). The patient had none of these conditions.
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.
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. Nossen, who practices in Norway — today's ECG uses the Cabrera Format.
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.
2] Conduction through the accessory pathway can be intermittent (with different degrees of pre-excitation), and affected by ischemia. 3] So a patient with WPW can have the pattern induced by ischemia, and there is also a report of a patient with pre-existing WPW which was “ablated” by myocardial infarction after an LAD occlusion.[4]
Blunt Trauma in a Child 40-something male in a head-on Motor Vehicle Collision and Splenic Injury == MY Comment, by K EN G RAUER, MD ( 10/10 /2022 ): == Highly interesting post by Dr. Smith regarding a 30-something male with multiple injuries from a motor vehicle accident. What are the ECG Findings of Cardiac Contusion?
Here is his ECG: There is no clear evidence of OMI or ischemia. This is guideline approved by both ACC/AHA and by European guidelines. == Comment by K EN G RAUER, MD ( 6/1/2022 ): == I found serial evaluation of sequential tracings in today's case to be subtle — yet highly insightful.
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.
Baseline bradycardia in endurance athletes limits the use of ß-blockers. These include: i ) Use of rate-slowing medication ( ie, ß-blockers, digoxin, verapamil/diltiazem, etc. ) ; ii ) Acute or recent infarction or ischemia; iii ) Hypothyroidism; iv ) Neurologic injury; v ) Electrolyte disturbance; and , vi ) Sleep apnea. 25, 2022 ).
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.
L/min, BP 107/65 mm Hg, HR 71 bpm LVEF 45%, no wall motion abnormality The patient had a complete neurologic recovery, proving once again that the patient is not dead until he/she is warm and dead. == MY Comment by K EN G RAUER, MD ( 2/8/2022 ): == I thought this to be an intriguing case for a number of reasons.
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?
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.
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. Can J Cardiol 2022 Kukla P, Jastrezebski M, Praefort W. What do you think?
That said there were no clinical symptoms or ECG findings suggestive of ongoing ischemia. Below in Figure-5 is a 10-minute continuous lead II recording on oral Flecainide, now showing sinus bradycardia without a single PVC! References: [1] 2022 ESC Guidelines for Ventricular Arrhythmias : Key Points - American College of Cardiology.
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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