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Bedside cardiac ultrasound showed moderately decreased LV function. CT of the chest showed no pulmonary embolism but bibasilar infiltrates. Discontinue all negative chronotropic agents, since the risk of torsade is much higher with bradycardia or pauses. See this post: How a pause can cause cardiacarrest 2.
This false electrical capture may have made cardiacarrest recognition difficult, and the re-arrest may have gone unrecognized for an unknown amount of time. The receiving staff suspects pulmonary embolism due to S1Q3T3 on the ECG and administers TPA. They are unable to feel a pulse and resume CPR.
In any case, there is bradycardia. It makes pulmonary embolism (PE) very likely. First, what kind of arrest was this? It was a PEA or bradyasystolic arrest , not a shockable rhythm. But it is bradyasystolic, so pulmonary embolism must be high on the differential. No shock was ever delivered. The RV is huge.
There is sinus bradycardia with one PVC. There is "Shark Fin morphology" I saw this and thought for certain that this was going to be an LAD or left main occlusion as etiology of arrest, and etiology of profound ST Elevation in I, II, aVL, and V3-V6, and ST depression in III, V1 and V2. pulmonary embolism, sepsis, etc.),
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