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No ischemia. Case continued Another ECG was recorded 3 hours later, still 1/10 pain: There is sinus bradycardia with RBBB. This is a conundrum, because it is clear that the patient is having an acute MI, the ECG is dynamic, but the pain is very mild and there is no ECG evidence of active transmural ischemia.
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?
The patient was referred immediately for cath which revealed RCA occlusion that was stented. 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. There is ST depression in V1.
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. Finally the OMI was realized.
Soon afterward, the patient’s symptoms return along with lightheadedness, bradycardia, and hypotension. The patient has also developed sinus bradycardia, which may result from right coronary artery ischemia to the SA node. Two stents were placed with resultant TIMI 3 flow.
I see the following: The rhythm is sinus bradycardia at ~55-60/minute. C ASE C onclusion : Timely cardiac cath was performed on today's patient — with successful reperfusion and stenting of his proximal LAD occlusion. = The PR and QRS intervals are both normal. ECG Blog #230 — How to compare serial ECGs.
A prehospital “STEMI” activation was called on a 75 year old male ( Patient 1 ) with a history of hyperlipidemia and LAD and Cx OMI with stent placement. 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. It was stented.
Here is his previous ECG: This was my interpretation of the first ECG: Sinus bradycardia with less than 1mm ST elevation in V4-V6, elevated compared to the previous ECG, suggestive of lateral MI. Both were stented. This is his first ECG in the department, which I saw as it was being printed: What do you think?
This middle aged male with h/o GERD but also h/o stents presented to the ED with chest pain. The computer called "Sinus Bradycardia" only (implying that everything else is normal. The overreading Cardiologist called it only "Sinus Bradycardia" with no other findings. The rhythm in Figure-1 is sinus bradycardia and arrhythmia.
Sinus bradycardia, normal conduction, normal axis, normal R wave progression, no hypertrophy. It was a 60yo with a history of stents to the circumflex and right coronary arteries, who presented with 9 hours of fluctuating central chest pain. What do you think? But it is still STEMI negative.
After many hours, the decided that it was appropriate to do an angiogram and they found a distal LAD occlusion which was opened and stented. Patient presentation is important This was a 60-something with acute chest pain: There is sinus bradycardia at a rate of 44. Why bradycardia? It was stented. STE60V3 = 2.5
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.
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.
Here are inferior leads, and aVL, magnified: A closer inspection of the inferior leads and aVL Sinus bradycardia. The patient was then taken to the cath lab an found to have a proximal RCA 100% thrombotic occlusion which was successfully stented. I had no history on the case and no prior ECG for comparison. What do you think?
60-something with h/o MI and stents presented with chest pain radiating to the back and nausea/vomiting. It was stented. The patient had a p rior h istory of MI + stents. This is sinus bradycardia. More likely, these T waves probably reflect ischemia of uncertain age. Time zero What do you think? Pericarditis?
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. This was stented. The corrected QT interval is extremely long, about 500 ms.
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