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Bedside cardiacultrasound showed moderately decreased LV function. 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. She was intubated. The plan: 1. Place temporary pacemaker 3.
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. She then had a 12-lead: What do you think?
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. If cardiacarrest from hypokalemia is imminent (i.e., He was managed medically with Clopidogrel.
There was no evidence bradycardia leading up to the runs of PMVT ( as tends to occur with Torsades ). If there had been — a temporary atrial pacemaker could have been considered as a way of increasing the heart rate to suppress a bradycardia-dependent arrhythmia ("overdrive pacing").
In any case, there is bradycardia. A bedside cardiacultrasound 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. Second: what does the ultrasound tell us about the condition? No shock was ever delivered. He was intubated.
Further history later: This patient personally has no further high risk features (syncope / presyncope), but her mother had sudden cardiacarrest in sleep. Regardless of further evaluation, she should avoid bradycardia, AV nodal blockers, Na channel blockers, and fevers. --If
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