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He was treated for infection and DKA and admission to hospital was planned. Important point: when there is diffuse subendocardial ischemia but no OMI, a wall motion abnormality will not necessarily be present. See this post: What do you think the echocardiogram shows in this case? That this is all demand ischemia is unlikely.
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.
A transthoracic echocardiogram showed an LV EF of less than 15%, critically severe aortic stenosis , severe LVH , and a small LV cavity. DISCUSSION: The 12-lead EKG EMS initially obtained for this patient showed severe ischemia, with profound "infero-lateral" ST depression and reciprocal ST elevation in lead aVR.
He was intubated in the field and sedated upon arrival at the hospital. 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. They shocked him twice before return of spontaneous circulation.
Again, it is common to have an ECG that shows apparent subendocardial ischemia after resuscitation from cardiac arrest, after defibrillation, and after cardioversion. and repeat the ECG, to see if the apparent ischemia persists. A third ECG was done about 25 minutes after the first: This shows resolution of all apparent ischemia.
When flow is restored, wall motion may completely recover so that echocardiogram does not detect the previous ischemia. Even when the serial troponins are negative, the ECG is critical to the diagnosis of ACS. This is not pericarditis because: a. Pain was typical for MI (substernal, not postional or sharp, resolved with NTG) b.
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.
He was admitted to the hospital for evaluation of these symptoms — but no ECG was done at that time. The patient’s angiogram should have been expedited, but the EKG change was not recognized as recurrence of transmural ischemia. The rest of the patient’s hospital stay was uneventful and he was eventually discharged.
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?
My interpretation was: RBBB with hyperacute T-waves in V4-V6 that are all but diagnostic of LAD occlusion vs. post ROSC ischemia. Formal Echocardiogram: Normal left ventricular size and wall thickness. The patient had ROSC and maintained it. A 12-lead ECG was obtained: What do you think?
The patient was promptly admitted to the hospital for further evaluation. A rapid echocardiogram was performed, revealing an ejection fraction of 20% with thinning of the anterior-apical walls. An initial electrocardiogram (ECG) is provided below. What do you think? What is the rhythm? The rate is 132 bpm.
Whether these EKGs show myocarditis, a normal variant, or something else, they are overall not typical of transmural ischemia of the anterior or high lateral walls. Additionally, a bedside echocardiogram showed no wall motion abnormality and normal LV function. Patient 1 remained in the hospital overnight.
The ECG shows sinus tachycardia with RBBB and LAFB, without clear additional superimposed signs of ischemia. Hopefully a repeat echocardiogram will be performed outpatient. Between 81-95% of life-threatening ventricular dysrhythmias and acute cardiac failure occur within 24-48 hours of hospitalization. No cardiac MRI was done.
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.
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.
However, an echocardiogram is a different test, also conducted for heart activity. Patients use them to observe their heart activity by themselves when they are not in the hospital. Electrocardiogram, echocardiogram, and some other tests are done for patients with cardiac arrest. ECG and EKG refer to the same thing.
Post by Smith, with short article by Angie Lobo ( [link] ), a third year intermal medicine resident at Abbott Northwestern Hospital Case A 30-something woman with no past history, who is very fit and athletic, presented with 1.5 It was late evening and the patient will be in the hospital overnight with a potentially very unstable LAD lesion.
He had been seen several weeks ago at an outside hospital for a similar issue and had been discharged home, presumably after unremarkable workup. This proves that the first one was, surprisingly, due to ischemia!! He was ultimately discharged after a brief, uncomplicated hospital course. Do NOT use them.
These findings are concerning for inferior wall ischemia with possible posterior wall involvement. His initial cTnI at the receiving hospital was 27 ng/mL, and no further troponins were measured thereafter. The morphology in V2 is also concerning and it appears that the ST segment is being pushed down, as in ST depression.
We see a regular tachycardia with a narrow QRS complex and no evidence of OMI or subendocardial ischemia. She had an echocardiogram which was normal. She reports that she is now unable to vagal out of her palpitations and is having shortness of breath and dull chest pain. Her initial EKG is below.
Another ECG was recorded 5 minutes later just before arrival at the hospital: Similar The patient was transported to a nearby suburban hospital with PCI capabilities while my partner cared for her. Here is the cath report: Echocardiogram: There is severe hypokinesis of entire LV apex and apical segment of all the walls.
Evidence of acute ischemia (may be subtle) vii. Clinical predictors of cardiac syncope at initial evaluation in patients referred urgently to general hospital: the EGSYS score. Background: Syncope is a common, potentially serious condition accounting for many hospital admissions. Left BBB vi. Pathologic Q-waves viii.
There is no evidence of infarction or ischemia. The patient was given furosemide and admitted to the hospital. Later, he underwent a formal echocardiogram: Very severe left ventricular enlargement (LVED diameter 7.4 There are nonspecific ST-T abnormalities. Troponin I was 0.054 ng/mL NT-ProBNP was 8316 (0-900 pg/mL). "
Cardiology services were consulted at a PCI capable hospital. The patient was started on heparin for possible NSTEMI vs demand ischemia. increasing stenosis, ischemia, volume changes, increased blood pressure, atrial fibrillation, etc.) Smith : these ECGs do NOT show subendocardial ischemia.
In this study of consecutive patients with LBBB who were hospitalized and had an echocardiogram, a QRS duration less than 170 ms (n = 262), vs. greater than 170 ms (n = 38), was associated with a significantly better ejection fraction (36% vs. 24%). Negative trops and negative angiogram does not rule out coronary ischemia or ACS.
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