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Here is the EMS ECG: Obviously massive diffuse subendocardial ischemia, with profound STD and STE in aVR Of course this pattern is most often seen from etoliogies other than ACS. The ECG only tells you there is ischemia, not the etiology of it. What do you think the echocardiogram shows? NTG drip started. Pain better still.
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. J Am Coll Cardiol.
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?
One very useful adjunct is ultrasound: Echo of his heart can distinguish aneurysm from acute MI by presence of diastolic dyskinesis, but it cannot distinguish demand ischemia from ACS. Furthermore, notice the well-formed Q-waves in inferior leads. These must raise suspicion of old MI with persistent ST elevation.
1.196 x STE60 in V3 in mm) + (0.059 x computerized QTc) - (0.326 x RA in V4 in mm) Third, one can do an immediate cardiac ultrasound. A bedside ultrasound was done by an emergency physician and simultaneously read by a cardiologist. greater than 23.4 is likely anterior STEMI). LV aneurysm is very different for inferior vs. anterior MI.
His response: “subendocardial ischemia. Smith : It should be noted that, in subendocardial ischemia, in contrast to OMI, absence of wall motion abnormality is common. See this case: what do you think the echocardiogram shows in this case? Anything more on history? POCUS will be helpful.” J Electrocardiol 2013;46:240-8 2.
So today i wanted to talk to you about what each heart test tells us about these different aspects of heart disease Tests that tell you about the heart as a pump The most commonly used test to assess the heart as a pump is an echocardiogram. This is an ultrasound (a bit like the type that we use on pregnant women to look at the baby).
This proves that the first one was, surprisingly, due to ischemia!! After rethinking the case, he remained concerned about ACS and subsequently performed a point-of-care ultrasound in order to evaluate for regional wall motion abnormality. A second troponin had been drawn 3 hours after arrival and was again less than 0.30ng/mL.
This strongly suggests reperfusing RCA ischemia. Troponins, echocardiogram An echocardiogram showed inferobasilar hypokinesis, further supporting a diagnosis of regional ischemia , likely of the area supplied by the RCA. There is also a Q-wave in III. There is also subtle STD in V3-V5. ng/ml (99th %-ile URL = 0.04
Normally, concavity in ST segments suggests absence of anterior ischemia (though concavity by itself is not reassuring - see this study ). His ED cardiac ultrasound (which is not at all ideal for detecting wall motion abnormalities, and is also very operator dependent for this finding) was significant for depressed global EF.
Case continued: All the physicians were very worried about LAD occlusion and recorded a couple bedside ultrasounds: This shows a profound apical and septal wall motion abnormality, perfectly consistent with LAD OMI. These ultrasounds confirm LAD occlusion. Pain will resolve with completed infarct or with resolution of ischemia.
ALL TROPS WERE UNDETECTABLE A formal ultrasound was done: Normal estimated left ventricular ejection fraction at rest. Next day, a stress echo was done: The exercise stress echocardiogram is normal. This ST-T wave appearance in the lateral chest leads of ECG #2 is consistent with L V “ S train” vs ischemia.
This case was provided by Spencer Schwartz, an outstanding paramedic at Hennepin EMS who is on Hennepin EMS's specialized "P3" team, a team that receives extra training in advanced procedures such as RSI, thoracostomy, vasopressors, and prehospital ultrasound. This entire case is not consistent with takotsubo. It can only be seen by IVUS.
However, with widespread ST depression, this could also be due to diffuse subendocardial ischemia. Everything is complicated by the arrest and hypotension: Is the ischemia caused by the instability, or the instability caused by the ischemia? What was the inciting factor? The diagnosis is in doubt. Plummer D et al.
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.
There is no evidence of infarction or ischemia. A bedside POC cardiac ultrasound was done: Findings: Decreased left ventricular systolic function. Later, he underwent a formal echocardiogram: Very severe left ventricular enlargement (LVED diameter 7.4 There are nonspecific ST-T abnormalities.
I suspect pulmonary edema, but we are not given information on presence of B-lines on bedside ultrasound, or CXR findings. The patient was started on heparin for possible NSTEMI vs demand ischemia. increasing stenosis, ischemia, volume changes, increased blood pressure, atrial fibrillation, etc.)
The clinical significance of ARCA-LCS lies in its potential to cause myocardial ischemia or sudden cardiac death, particularly under physical exertion. Transthoracic echocardiogram, bilateral carotid Doppler ultrasound, and electrocardiogram were normal. No previous history of hypertension or diabetes.
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