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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. A bedside cardiac ultrasound performed by a true EM expert (Robert Reardon, who wrote the cardiac ultrasound chapter in Ma and Mateer) showed an inferior wall motion abnormality.
Bedside cardiac ultrasound showed moderately decreased LV function. Discontinue all negative chronotropic agents, since the risk of torsade is much higher with bradycardia or pauses. She was intubated. CT of the chest showed no pulmonary embolism but bibasilar infiltrates. The plan: 1. Place temporary pacemaker 3.
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.
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.
In any case, there is bradycardia. There is ST depression beyond the end of the wide QRS in I, II, aVF, and V4-V6, diagnostic of with subendocardial ischemia. A bedside cardiac ultrasound was recorded: Here is a still image of the echo: The red arrows outline the right ventricle and the yellow arrows outline the left ventricle chamber.
However the patient continued to have chest pain and bedside ultrasound showed hypokinesis of the septum with significantly reduced LVEF. Possible mechanisms of ventricular arrhythmias elicited by ischemia followed by reperfusion. The receiving emergency physician consulted with interventional cardiology who stated there was no STEMI.
Dr. Nossen performed a bedside ultrasound which was interpreted as normal. 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.
Patient presentation is important This was a 60-something with acute chest pain: There is sinus bradycardia at a rate of 44. To me, this makes the ECG nearly diagnostic of ischemia, though if it is LAD occlusion, there should be ST depression in III and aVL, so it is a bit confusing. Why bradycardia? 100% distal LAD occlusion.
Bedside ultrasound showed no effusion and moderately decreased LV function, with B-lines of pulmonary edema. There is also bradycardia. Bradycardia puts patients at risk for "pause-dependent" Torsades de Pointes. Angio had shown some acute disease in the saphenous vein graft to the posterior descending artery off of the RCA.
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.
Her bedside cardiac ultrasound was normal We decided to cardiovert her since the time of onset was very recent. Baseline bradycardia in endurance athletes limits the use of ß-blockers. But when you see this, you should suspect that the AV node is not well. I signed her out to one of my partners.
Check : [vitals, SOB, Chest Pain, Ultrasound] If the patient has Abdominal Pain, Chest Pain, Dyspnea or Hypoxemia, Headache, Hypotension , then these should be considered the primary chief complaint (not syncope). Evidence of acute ischemia (may be subtle) vii. Aortic Dissection, Valvular (especially Aortic Stenosis), Tamponade.
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