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Smith comment: The patient was lucky to have a cardiacarrest. By undergoing an arrest, providers became aware of his OMI which had not been noticed on his diagnostic ECG, and he thus has a chance at some myocardial salvage. Had he not had one, he would have sat in the waiting room until his entire myocardium at risk infarcted.
STE limited to aVR is due to diffuse subendocardial ischemia, but what of STE in both aVR and V1? The additional ST Elevation in V1 is not usually seen with diffuse subendocardial ischemia, and suggests that something else, like STEMI from LAD occlusion, could be present. Was this: 1) ACS with ischemia and spontaneous reperfusion?
There is profound LVH with anterolateral ST elevation and reciprocal ST depression in II, III, aVF, and ST depression in V5 and V6 that could all be secondary to LVH or could represent ischemia superimposed on the repolarization abnormalities of LVH: note that wherever there is ST depression, it is associated with a very high voltage R-wave.
This was interpreted by the treating clinicians as not showing any evidence of ischemia. Echocardiogram showed LVEF 66% with normal wall motion and normal diastolic function. However, he did not remember much from the day of the arrest. He was intubated in the field and sedated upon arrival at the hospital.
However, an echocardiogram is a different test, also conducted for heart activity. CardiacarrestCardiacarrest is a medical emergency in which the heart stops pumping blood to the body. Electrocardiogram, echocardiogram, and some other tests are done for patients with cardiacarrest.
This may result in ischemia (lack of oxygen to the heart muscle), causing parts of the heart to weaken and enlarge. Echocardiogram An echocardiogram uses sound waves to produce a detailed image of the heart, allowing doctors to see the size of the heart chambers and how well the heart is pumping blood.
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.
See this post: How a pause can cause cardiacarrest 2. 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. The plan: 1. Place temporary pacemaker 3.
It should be known that each category can easily manifest the generic subendocardial ischemia pattern. In general, subendocardial ischemia is a consequence of global supply-demand mismatch that usually ameliorates upon addressing, and mitigating, the underlying cause. What’s interesting is that the ECG can only detect ischemia.
Normally, concavity in ST segments suggests absence of anterior ischemia (though concavity by itself is not reassuring - see this study ). I think a good start would be a posterior EKG and a high quality contrast echocardiogram read by an expert. In there ECG evidence of possible ongoing ischemia? (ie,
hours ECG: Not much change hs troponin I peaks at 500 ng/L 8 hours Next morning Urine drug screen: Amphetamine, Methamphetamine, Fentanyl, Fentanyl metabolite Formal Bubble Contrast Echocardiogram: Indications for Study: Silent Ischemia. SUMMARY Normal left ventricular cavity size. Normal estimated left ventricular ejection fraction.
Two recent interventions have proven in randomized trials to improve neurologic survival in cardiacarrest: 1) the combination of the ResQPod and the ResQPump (suction device for compression-decompression CPR -- Lancet 2011 ) and 2) Dual Sequential defibrillation. Formal Echocardiogram: Normal left ventricular size and wall thickness.
ST depression is common BOTH after resuscitation from cardiacarrest and during atrial fib with RVR. Again, it is common to have an ECG that shows apparent subendocardial ischemia after resuscitation from cardiacarrest, after defibrillation, and after cardioversion. The patient was cardioverted. This was done.
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.
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.
It is apparently fortunate that she had a cardiacarrest; otherwise, her ECG would have been ignored. Here is the cath report: Echocardiogram: There is severe hypokinesis of entire LV apex and apical segment of all the walls. She was defibrillated and resuscitated. I need to innoculate you against the subsequent opinions below.
Formal echocardiogram showed normal EF, no wall motion abnormalities, no pericardial effusion. The patient proceeded to cath where all coronaries were described as normal with no evidence of any CAD, spasm, or any other abnormality. No more troponins were done. He was found to be influenza positive. 1849 after cath: Brugada pattern is gone!
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.
An echocardiogram was done. These include ( among others ) — acute febrile illness — variations in autonomic tone — hypothermia — ischemia-infarction — malignant arrhythmias — cardiacarrest — and especially Hyperkalemia. Is there also Brugada? Here is the result: The estimated left ventricular ejection fraction is 50 %.
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." NOTE #3: In the context of a long QTc or ischemia — the finding of ST segment and/or T wave alternans may predict the occurrence of malignant ventricular arrhythmias. The echo was normal.
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