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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. She was intubated. Bedside cardiac ultrasound showed moderately decreased LV function. The plan: 1. Place temporary pacemaker 3.
This middle-aged patient presented with SOB, weakness, and mild pulmonary edema. There are 3 etiologies I always think of with bradycardia and AV block: 1. There was no evidence of ischemia. We are not told how ischemia has been ruled out in this case. She previously had Atrial fibrillation with LBBB. Hyperkalemia.
The ECG shows sinus tachycardia with RBBB and LAFB, without clear additional superimposed signs of ischemia. Q waves in association with RBBB are usually not seen in anterior leads unless there is pulmonary hypertension or anterior infarction. Chest trauma was suspected on initial exam.
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. It makes pulmonary embolism (PE) very likely. The small LV implies very low LV filling pressures, which implies low pulmonary venous pressure. Summary: 1.
Was there pulmonary edema? There is a junctional bradycardia. Furthermore, there are T-wave changes in V2 and V3 which are highly suggestive of ischemia, but difficult to localize: anterior? Then they were worried about sepsis as an etiology of hypotension. Not mentioned in physicians' notes. She was taken to the cath lab.
But when the clinical presentation is sepsis, one must entertain the possibility that the ST elevation is due to demand ischemia, or some other process, and exacerbated by tachycardia. The estimated pulmonary artery systolic pressure is 37 mmHg + RA pressure. Normal estimated left ventricular ejection fraction lower limits of normal.
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. Bradycardia puts patients at risk for "pause-dependent" Torsades de Pointes.
Evidence of acute ischemia (may be subtle) vii. PVCs N ot generally considered abnormal ECG findings: Isolated PAC, First Degree AV Block, Sinus bradycardia at a rate of 35-45, and Nonspecific ST-T abnormalities (even if different from a previous ECG). Aortic Dissection, Valvular (especially Aortic Stenosis), Tamponade. Left BBB vi.
she had severe pulmonary edema. This is the etiology of the blood from her nose and mouth (frothy bloody pulmonary edema) This is what frothy bloody pulmonary edema looks like. Subarachnoid hemorrhage causes extreme central catecholamine output, resulting in stress cardiomyopathy, just like takotsubo. From this site.
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