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Bedside cardiac ultrasound showed moderately decreased LV function. It should be kept in mind that on occasions, beta-one agonist can result in increased ventricular ectopy e.g., in severe myocardial ischemia (by increasing myocardial demand), or sometimes with congenital long-QT syndrome. She was intubated.
Smith comment: This patient did not have a bedside ultrasound. Had one been done, it would have shown a feature that is apparent on this ultrasound (however, this patient's LV function would not be as good as in this clip): This is recorded with the LV on the right. What should be done? Should the cath lab be activated?
He arrived in the ED and had an immediate bedside cardiac ultrasound while this ECG was being recorded. The bedside ultrasound (video not available) reportedly showed only a slightly reduced LV function. The patient was given 6mg, then 12 mg, of adenosine, without a change in the rhythm. Here is the ECG: What do you think?
His response: “subendocardial ischemia. Smith : It should be noted that, in subendocardial ischemia, in contrast to OMI, absence of wall motion abnormality is common. With the history of Afib, CTA abdomen was ordered to r/o mesenteric ischemia vs ischemic colitis vs small bowel obstruction. Anything more on history?
Her bedside cardiac ultrasound was normal We decided to cardiovert her since the time of onset was very recent. The Role of Sinus Arrhythmia: I found it interesting to compare the long lead II rhythm strips in the 3 serial tracings from today’s case ( Figure-1 ). But when you see this, you should suspect that the AV node is not well.
Here was his prehospital ECG, which I viewed immediately while the resident performed cardiac ultrasound: What do you think? Here is the cardiac ultrasound which the resident performed as I viewed the ECG: This shows a huge pericardial effusion. Therefore, we performed ultrasound-guided pericardiocentesis. Is is sinus?
A bedside cardiac ultrasound was performed with a parasternal long axis view demonstrated below: There is a large pericardial effusion with collapse of the right ventricle during systole. Alternation in ST segment appearance ( or in the amount of ST elevation or depression ) — is often linked to ischemia. She has already had syncope.
However, he suddenly developed a series of malignant ventricular arrhythmias. Below are printouts of some of the arrhythmias recorded. There is no definite evidence of acute ischemia. (ie, This time, the arrhythmia did not spontaneously terminate — but rather degenerated to VFib, requiring defibrillation.
There are three mechanisms of arrhythmia: automatic, re-entry, and triggered. The most common triggered arrhythmia is Torsades de Pointes. It is a benign arrhythmia which requires no specific treatment. Possible mechanisms of ventricular arrhythmias elicited by ischemia followed by reperfusion. What is the rhythm?
Bedside ultrasound showed no effusion and moderately decreased LV function, with B-lines of pulmonary edema. If there is polymorphic VT with a long QT on the baseline ECG, then generally we call that Torsades, but Non-Torsades Polymorphic VT can result from ischemia alone. He was managed medically with Clopidogrel. mmol/L (range 0.11.7
This was diagnosed by IVUS (intravascular ultrasound) as a ruptured plaque. This was clearly severe subepicardial ischemia causing ST Elevation, but it was not of a long enough duration to result in measurable infarct. Although there is no long lead rhythm strip — it is noteworthy that there is marked sinus arrhythmia in ECG #1.
There is no evidence of infarction or ischemia. A bedside POC cardiac ultrasound was done: Findings: Decreased left ventricular systolic function. There is a large peaked P-wave in lead II (right atrial enlargement) There is left axis deviation consistent with left anterior fascicular block. There are nonspecific ST-T abnormalities.
We computed a Vascular Disease (VasD) score, integrating the presence of carotid plaque (CP) on carotid ultrasound, known coronary artery disease (CAD), and myocardial ischemia (MyI). Subsequently, patients were followed for 5.5 Survival curves depicted a rising risk of the outcome corresponding to increasing VasD scores (Figure 1).Conclusions:The
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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