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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. Smith, this can be accomplished by either using beta-one agonists or temporary transvenous pacing. J Am Coll Cardiol.
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.
My written interpretation on a tracing such as this one would read, "Marked LVH and 'strain' and/or ischemia — with need for clinical correlation." BOTTOM LINE: ECG changes of LV "strain" and/or ischemia that we see on today's initial ECG — were not present 9 years earlier. Cardiac cath showed normal coronary arteries.
In any case, the ECG is diagnostic of severe ischemia and probably OMI. So this could be myocarditis but in my opinion needs an angiogram before making that diagnosis. == Dr. Nossen Comment/Interpretation: Evaluation of ischemia on an ECG can be very challenging. Concordant STE of 1 mm in just one lead or 2a.
A rapid echocardiogram was performed, revealing an ejection fraction of 20% with thinning of the anterior-apical walls. Learning Point: Concordant ST segment elevation can arise from profound ischemia triggered by ventricular tachycardia (VT), or it may represent an exaggerated basal ST change accompanying tachycardia.
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? Am J Med 2019, 132(5):622-630. Anything more on history? POCUS will be helpful.”
See this case, where a patient with BTWI morphology and dramatic EKG changes within minutes is diagnosed with myocarditis: [link] com/2019/07/what-does-this- ecg-with-significant-st.html EKG 3 also has a saddleback morphology in V2, which is only rarely due to OMI. Still, such dramatic changes cannot be overlooked.
or basilar ischemia. Echocardiogram was obtained and showed mild LVH without regional wall motion abnormality. Rather than loss of both a J wave and S wave — there is a "slur" ( J-point equivalent ) in lead V2 of ECG #2 ( See My Comment in the November 14, 2019 post for illustration of T-QRS-D ). ng/mL and 0.10
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. JACC 2019 Sep 10;74(10):1290-1300. There is also a Q-wave in III. ng/ml (99th %-ile URL = 0.04
Does this mean that the ST depression in V3 represents "anterior" subendocardial ischemia, and not posterior OMI? Echocardiogram: The estimated left ventricular ejection fraction is 34% Regional wall motion abnormality-lateral, akinetic. non-occlusive ischemia) 2. Thus, they have much less voltage. They have ZERO ST Elevation.
I have ordered an echocardiogram which will be done today, after that patient can be discharged to home with follow-up in 2 to 3 months." Not all forms of idiopathic VT are predictable based on their ECG appearance ( Anderson et al, 2019 ). The echo was normal. Learning points 1.
These findings are concerning for inferior wall ischemia with possible posterior wall involvement. Unfortunately there is no echocardiogram accessible because the patient checked himself out of the hospital in order to get back to his home state before it could be completed. No significant changes, ongoing pain.
An echocardiogram was done. These include ( among others ) — acute febrile illness — variations in autonomic tone — hypothermia — ischemia-infarction — malignant arrhythmias — cardiac arrest — and especially Hyperkalemia. Is there also Brugada? Here is the result: The estimated left ventricular ejection fraction is 50 %.
2 days later This is a typical LVH pattern, without ischemia Patient underwent 4 vessel CABG. After discussing all of the above with ED staff, we have made a decision to get stat echocardiogram and assess overall LV function and wall motion abnormalities and defer cath lab activation at the time."
Here is the cath report: Echocardiogram: There is severe hypokinesis of entire LV apex and apical segment of all the walls. Hospital Course The patient was taken emergently to the cath lab which did not reveal any significant coronary artery disease, but she was noted to have reduced EF consistent with Takotsubo cardiomyopathy.
There is no evidence of infarction or ischemia. Later, he underwent a formal echocardiogram: Very severe left ventricular enlargement (LVED diameter 7.4 E CG # 2 in Figure-1 is from the October 16, 2019 post on Dr. Smith’s Blog. A follow-up ECG was done in this October 16, 2019 case , and did indeed show WPW.
Pain will resolve with completed infarct or with resolution of ischemia. ECG recorded at 7 hours All active ischemia is gone. Pain will resolve not just with resolution of ischemia, but with completion of infarction. This looks like infarct completion. Patient was placed on a nitro drip and pain remained under control.
A formal echocardiogram was completed the next day and again showed a normal ejection fraction without any focal wall motion abnormalities to suggest CAD. Cardiology was consulted and they agreed that the EKG had an atypical morphology for STEMI and did not activate the cath lab. Heart Rhythm, 15(9): 1394-1401. [7]
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