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He was defibrillated, but they also noticed that he was being internally defibrillated and then found that he had an implantable ICD. He was unidentified and there were no records available After 7 shocks, he was successfully defibrillated and brought to the ED. Tachycardia exaggerates ST Elevation in LBBB and Paced rhythm 5.
CT of the chest showed no pulmonary embolism but bibasilar infiltrates. Because she has cardiomyopathy and ventricular dysrhythmias, the pacer included an Implanted Cardioverter-Defibrillator (ICD) Echo 6 days later after CRT: Normal estimated left ventricular ejection fraction. Even with tachycardia and a paced QRS duration of ~0.16
She was successfully revived after several rounds of ACLS including defibrillation and amiodarone. An Initial ECG was performed: Initial ECG: Sinus tachycardia with prolonged QT interval (QTc of 534 ms by Bazett). On arrival to the ED the patient was intubated with normal vital signs. No ischemic ST changes. Teaching Points: 1.
Over the past years, patients with tetralogy of Fallot (TOF) have experienced numerous improvements in different treatment modalities consisting of a mixture of surgical procedures, transcatheter interventions including ablation therapy, and implantable cardioverter-defibrillator implantation procedures.
This usually represents posterior OMI, but in tachycardia and especially after cardiac arrest, this could simply be demand ischemia, residual subendocardial ischemia due to the low flow state of the cardiac arrest. This prompted cath lab activation. On arrival to the ED, this ECG was recorded: What do you think?
Thrombus can sometimes occur when there is a central venous catheter or a multiple pacemaker or defibrillator leads there that can cause thrombus formation. Right atrial hypertrophy as in tricuspid stenosis, pulmonary stenosis and pulmonary hypertension. But in a VSD with pulmonary hypertension A wave is not prominent.
It was reportedly a PEA arrest; there was no recorded V Fib and no defibrillation. The morphology of V2-V4 is very specific in my experience for acute right heart strain (which has many potential etiologies, but none more common and important in EM than acute pulmonary embolism). CT angiogram showed extensive saddle pulmonary embolism.
Bedside ultrasound showed no effusion and moderately decreased LV function, with B-lines of pulmonary edema. At cath, he immediately had incessant Torsades de Pointes requiring defibrillation 7 times and requiring placement of a transvenous pacer for overdrive pacing at a rate of 80. He appeared to be in shock.
The abnormal heart rhythms can further lead to death because of ventricular tachycardia and ventricular fibrillation. These issues can only be addressed in an ICCU (Intensive Coronary Care Unit) setting, where temporary pacemakers and defibrillators are available.
We rapidly defibrillated her, and with return of normal sinus rhythm. Several minutes later the patient developed V-fib again > 200J defibrillation with return to NSR. Rapid sequence intubation was performed for airway protection in setting of recurrent V-fib and defibrillations. Chest X-ray also showed pulmonary edema.
Smith comments : Wide complex tachycardia. The differential diagnosis of WCT is: 1) Sinus tachycardia with "aberrancy" (in this case RBBB and LAFB), but there are no P-waves and the QRS morphology is not typical of simple RBBB/LAFB. Also, if the rate is constant, not wavering up and down, it is highly unlikely to be sinus tachycardia.
There was never ventricular fibrillation (VF) or ventricular tachycardia (VT), no shockable rhythm. she had severe pulmonary edema. This is the etiology of the blood from her nose and mouth (frothy bloody pulmonary edema) This is what frothy bloody pulmonary edema looks like. There is sinus tachycardia at ~115/minute.
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