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= Case Presentation by K EN G RAUER, MD ( 5/5 /2023 ): — Edits by Drs. The "good" news — Treatment with naloxone will probably resolve the bradycardia. Meyers & Smith. = Dr. Smith was reading ECGs — and he sent myself and Dr. Meyers the tracing shown in Figure-1. At the time we did not yet know the history. What do YOU think?
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
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.
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 ).
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?
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?
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?
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.
to 1828 msec. ) — which corresponds to a variation in the rate of sinus bradycardia from 36-to-33/minute. This makes sense given that the underlying rhythm in today's case appears to be marked sinus bradycardia and arrhythmia , with a ventricular escape rhythm appearing when the SA node rate drops below 33/minute.
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. Subendocardial ischemia does not localize.
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 ).
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. The ECG does not show any signs of ischemia. True Positive ECG#2 : Also sinus rhythm. There is ST depression in V1.
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.
That said — obvious findings include: i ) Marked bradycardia! — This suggests ischemia of uncertain duration. A DDENDUM ( 10/28/2023 ) : This 15 -minute ECG Video ( M edia P EARL # 52) — Reviews the 3 Types of 2nd-Degree AV Block — plus — the hard-to-define term of "high-grade" AV block. be regular! —
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.
Here was my answer: "Not ischemia. 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. The patient has acute chest pain. What do you think? Maybe HOCM or another form of LVH. I would not activate cath lab.
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.
My Comment by K EN G RAUER, MD ( 3/15 /2023 ): = I found today’s case highly instructive in highlighting a number of important aspects regarding the presentation and initial treatment of a patient who presents to the ED with new AFib. Baseline bradycardia in endurance athletes limits the use of ß-blockers.
The patient later settled into sinus bradycardia. The amiodarone was discontinued and the patient did well. == MY Comment , by K EN G RAUER, MD ( 6/23 /2023 ): == From an academic standpoint — I love WCT ( W ide- C omplex T achycardia ) rhythms.
To improve visualization — I've digitized the original ECG using PMcardio ) MY Thoughts on the ECG in Figure-1: This is a challenging tracing to interpret — because there is marked bradycardia with an irregular rhythm and a change in QRS morphology. Figure-1: The initial ECG in today's case. ( The QRS complex is wide ( ie, >0.10
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 ).
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. 2004 = My Comment by K EN G RAUER, MD ( 1/21 /2023 ): = I thought today's case by Drs.
There is ST elevation in 9/12 leads with ST depression only seen in lead aVR>V1 ( ie, virtually the opposite of what is seen with diffuse subendocardial ischemia in which there is diffuse ST depression except for ST elevation in aVR>V1 ).
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.
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! You have given IV MgSO4 a fast acting -blocker and IV amiodarone bolus and infusion. No PVCs are seen.
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