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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. Even with tachycardia and a paced QRS duration of ~0.16 J Am Coll Cardiol.
This is ischemic ST depression, and could be due to increasing tachycardia, with a heart rate over 130, but that is unlikely given that the patient is now complaining of crushing chest pain and that there was tachycardia all along. See this post: What do you think the echocardiogram shows in this case? Aslanger's pattern.
He was rushed by residents into our critical care room with a diagnosis of STEMI, and they handed me this ECG: There is sinus tachycardia with ST elevation in II, III, and aVF, as well as V4-V6. ACS and STEMI generally do not cause tachycardia unless there is cardiogenic shock. He had this ECG recorded. Are the lungs clear?
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. While the initial impression might not immediately suggest ventricular tachycardia (VT), a closer examination raises suspicion. The initial troponin T level was measured at 30 ng/L. What is the rhythm?
The ECG shows sinus tachycardia with RBBB and LAFB, without clear additional superimposed signs of ischemia. Hopefully a repeat echocardiogram will be performed outpatient. The Initial ECG in Today's Case: As per Dr. Meyers — the initial ECG in today's case shows sinus tachycardia with bifascicular block ( = RBBB/LAHB ).
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.
Precordial ST depression may be subendocardial ischemia or posterior STEMI. Notice there is tachycardia. I have warned in the past that one must think of other etiologies of ischemia when there is tachycardia. V4-V6, is much more likely to be posterior than subendocardial ischemia. There is no ST elevation.
EKG, cardiac enzymes, and Initial echocardiogram(TTE) was unremarkable. Stress echocardiogram ruled out myocardial ischemia. However, symptoms resolved spontaneously, cardiac workup paused and he was monitored conservatively with serial Echocardiogram(TTE) until onset of dyspnea 3 years later.
She underwent exercise echocardiogram in mid October where she exercised for nearly 7 minutes on the standard Bruce protocol and had typical anginal pain and shortness of breath. Baseline echocardiogram showed moderate LV systolic dysfunction with no wall motion abnormalities. There is inferoseptal hypokinesis. link] Shvilkin et al.
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.
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. The patient had none of these conditions. It was stented.
EKG initially negative but repeat shows a few T wave abnormalities… There is a chance this could be non-cardiac pain” At 1518, an echocardiogram showed normal LV size and systolic function with hypokinesis of the mid and distal anterior wall and the mid and distal septum.
His prehospital ECG showed "inferior" ST depression and high voltage, with tachycardia. I suspected no OMI, that this could be due to LVH plus tachycardia. Conclusion: Type II MI probable due to hypoxia and tachycardia from resp arrest and amphetamine use. On arrival to the ED, the patient was diaphoretic, tachycardic.
We see a regular tachycardia with a narrow QRS complex and no evidence of OMI or subendocardial ischemia. The differential of a regular narrow QRS tachycardia is sinus tachycardia, SVT, and atrial flutter with regular conduction. Now the patient is in sinus tachycardia. She had an echocardiogram which was normal.
Here is his 12-lead: There is a wide complex tachycardia with a rate of 257, with RBBB and LPFB (right axis deviation) morphology. Read about Fascicular VT here: Idiopathic Ventricular Tachycardias for the EM Physician Case Continued He was completely stable, so adenosine was administered. See Learning point 1 below. Learning points 1.
However, an echocardiogram is a different test, also conducted for heart activity. A fast heartbeat is called tachycardia, while a slow heartbeat is called bradycardia in medical terms. Electrocardiogram, echocardiogram, and some other tests are done for patients with cardiac arrest. ECG and EKG refer to the same thing.
Prior ECG available on file from 2 months before: We do not know the clinical events happening during this ECG, but there is borderline tachycardia, PVCs, and likely some evidence of subendocardial ischemia with small STDs maximal in V5-6/II, slight reciprocal STE in aVR. Notice the normal precordial T waves.
Otherwise vitals after intubation were only notable for tachycardia. An initial EKG was obtained: Computer read: sinus tachycardia, early acute anterior infarct. A formal echocardiogram was completed the next day and again showed a normal ejection fraction without any focal wall motion abnormalities to suggest CAD.
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. Sinus Tachycardia ( common in any trauma patient. ). Is there also Brugada? Right ventricular prominence.
Here was his ED ECG: There is sinus tachycardia (rate about 114) with nonspecific ST-T abnormalities. There is no evidence of infarction or ischemia. Later, he underwent a formal echocardiogram: Very severe left ventricular enlargement (LVED diameter 7.4 There are nonspecific ST-T abnormalities. So what is it?
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.
If the patient has Abnormal Vital Signs (fever, hypotension, tachycardia, or tachypnea, or hypoxemia), then these are the primary issue to address, as there is ongoing pathology which must be identified. Evidence of acute ischemia (may be subtle) vii. Most physicians will automatically be worried about these symptoms. Left BBB vi.
The status of the patients chest pain at this time is unknown : EKG 1, 1300: There is sinus tachycardia and artifact of low and high frequency. However, there is also significant tachycardia , with heart rate of 116, and known hypoxia. The patient was started on heparin for possible NSTEMI vs demand ischemia.
During observation in the ED the patient had multiple self-terminating runs of Non-Sustained monomorphic Ventricular Tachycardia (NSVT). That said there were no clinical symptoms or ECG findings suggestive of ongoing ischemia. This patient very likely has some form of idiopathic ventricular tachycardia.
This ECG was recorded: It is difficult to appreciate P-waves, but I believe this is sinus tachycardia. Time 7 hours lead reversal There is limb lead reversal (QRS in I and aVL are now inverted), but nevertheless one can see that the ischemia appears to have resolved. He was put on BiPAP. A Chest X-ray did not show pulmonary edema.
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