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It is easy to say pericarditis in such a case. young male no risk factors and ST-elevation in several leads) As Dr. Smith has emphasized many times you diagnose pericarditis at your patient's and your own peril. With normal EF the tachycardia is not compensatory. Version 1 was not trained to detect myo- or pericarditis.
An Initial ECG was performed: Initial ECG: Sinus tachycardia with prolonged QT interval (QTc of 534 ms by Bazett). She was admitted to the ICU where subsequent ECGs were performed: ECG at 12 hours QTc prolongation, resolution of T wave alternans ECG at 24 hours Sinus tachycardia with normalized QTc interval. No ischemic ST changes.
These latter findings are typical of pericarditis, but pericarditis never has reciprocal ST depression. Usually with pericarditis and myocarditis — hyperacute T waves (HATW) are not present. NOTE #1: Sinus tachycardia is not usually seen in an uncomplicated acute MI. This is OMI until proven otherwise.
MY Interpretation of Today's Initial ECG: I've labeled key findings in Figure-2 for today's initial ECG: The rhythm is sinus tachycardia at ~105/minute. The sinus tachycardia is a definite concern that something acute may be ongoing. Figure-2: I've labeled t he initial ECG. All intervals ( PR, QRS, QTc ) are normal.
Here was the ECG: There is sinus tachycardia. Well, don't we see diffuse ST Elevation in Myo-pericarditis (with STD in aVR)? This was sent by a reader. A previously healthy 53 yo woman was transferred to a receiving hospital in cardiogenic shock. and K was normal. This is "Shark Fin" morphology. So this is STEMI, right? Which artery?
She was diagnosed with pericarditis and spent one day in the hospital without events. Much more classic findings of pericarditis. Learning Points: Pericardial effusion is a key piece of information for the diagnosis and prognosis of pericarditis. Another ECG was performed, and this time was noted to be markedly abnormal.
Other than tachycardia, Other than slight tachycardia, vitals were within normal limits (including oxygen saturation). As always, takotsubo cardiomyopathy and focal pericarditis can mimic OMI, but takotsubo almost never mimics posterior MI, and both are diagnoses of exclusion after a negative cath. Is that normal?
We can see enough to make out that the rhythm is sinus tachycardia. Tachycardia is unusual for OMI, unless the patient is in cardiogenic shock (or getting close). A bedside ultrasound should be done to assess volume and other etiologies of tachycardia, but if no cause of type 2 MI is found, the cath lab should be activated NOW.
The ECG shows sinus tachycardia, a narrow, low voltage QRS with alternating amplitudes, no peaked T waves, no QT prolongation, and some minimal ST elevation in II, III, and aVF (without significant reciprocal STD or T wave inversion in aVL). It is difficult to tell if there is collapse during diastole due to the patient’s tachycardia.
They include myocardial ischemia, acute pericarditis, pulmonary embolism, external compression due to mass over the right ventricular outflow tract region, and metabolic disorders like hyper or hypokalemia and hypercalcemia. 2020 Sep;31(9):2474-2483. J Cardiovasc Electrophysiol. Gourraud JB, Barc J, Thollet A, Le Marec H, Probst V.
The relationship between J wave and ventricular tachycardia during Takotsubo cardiomyopathy. Internat J Arrhyth 2020 Uesako H, Fukikawa H, Hashimoto S, et al. Prominent J waves and ventricular fibrillation caused by myocarditis and pericarditis after BNT162b2 mRNA COVID-19 vaccination.
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