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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.
The ECG shows sinus tachycardia with RBBB and LAFB, without clear additional superimposed signs of ischemia. ECG of pneumopericardium and probable myocardial contusion shows typical pericarditis Male in 30's, 2 days after Motor Vehicle Collsion, complains of Chest Pain and Dyspnea Head On Motor Vehicle Collision. ST depression.
There is sinus tachycardia. Sinus tachycardia, which exaggerates ST segments and implies that there is another pathology. I have always said that tachycardia should argue against acute MI unless there is cardiogenic shock or 2 simultaneous pathologies. PR depression, which suggests pericarditis 4.
Circulation: Arrhythmia and Electrophysiology, Ahead of Print. Colchicine did not prevent atrial arrhythmia recurrence at 2 weeks (31% versus 32%; hazard ratio [HR], 0.98 [95% CI, 0.59–1.61];P=0.92) Postablation chest pain consistent with pericarditis was reduced with colchicine (4% versus 15%; HR, 0.26 [95% CI, 0.09–0.77];P=0.02)
This is the proposed mechanism of precipitation of arrhythmias in Brugada syndrome during febrile episodes. There is a potential risk for drug challenge in that life threatening ventricular arrhythmias could be precipitated. This leads to shortening of action potential duration. With proper precautions, risk can be reduced.
I completely agree with Dr. Nossen that in this patient with new CP and sinus tachycardia with LAHB — that the T waves in each of the inferior leads are hyperacute ( ie, clearly disproportionately "bulky" given size of the QRS in these leads ). — and which other patient(s) need to be seen as soon as possible to figure out what is going on?
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.
He has a family history concerning for arrhythmia. Given the circumstances of his car crash, we presume it was due to an underlying arrhythmia. He has a family history concerning for arrhythmia with his father requiring some sort of device (PPM, ICD, unclear) at a young age. ST depression. Myocardial Contusion?
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.
While traditionally described as “benign early repolarization”, they have been associated with J wave syndromes along with Brugada syndrome, causing ventricular arrhythmias (1, 2). The relationship between J wave and ventricular tachycardia during Takotsubo cardiomyopathy. Indian Pacing Electrophysiol J 2004 Antzelevitch C, Yan G.
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