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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. Neverthelss, his anterior wall was saved and he had normal ejection fraction without heartfailure.
He denied any known medical history, specifically: coronary artery disease, hypertension, dyslipidemia, diabetes, heartfailure, myocardial infarction, or any prior PCI/stent. Breath sounds were clear in all lung fields. No appreciable skin pallor. He reported to be a social drinker, but used tobacco products daily.
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?
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. Heartfailure leading to death was related to all subclasses of PVC.
Case submitted by Andrew Grimes, Advanced Care paramedic, with additions from Jesse McLaren and Smith An 84-year-old male with a notable cardiac history (CABG, multiple stents) woke at 0500hrs with pressure in his chest, diaphoresis, and light-headedness. They end up with high mortality and needless heartfailure.
Within ten minutes, she developed bradycardia, hypotension, and ST changes on monitor. Bradycardia and heart block are very common in RCA OMI. After stent deployment, we often see improvement in the ST-T within seconds or minutes. Here is the final angiogram following placement of a stent in the ostial RCA.
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