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A patient had a cardiac arrest with ventricular fibrillation and was successfully defibrillated. IF the initial ECG following successful defibrillation shows evidence of acute OMI — such patients have much to gain from immediate cath with PCI. The proof of this is that only 5% of patients enrolled had acute coronary occlusion.
(MedPage Today) -- Not all defibrillator pad positions may work equally well for patients with shockable out-of-hospital cardiac arrest. JAMA Network Open) Medical therapy for aortic stenosis? Early clinical data on evogliptin were disappointing.
Again, it is common to have an ECG that shows apparent subendocardial ischemia after resuscitation from cardiac arrest, after defibrillation, and after cardioversion. The estimated left ventricular ejection fraction is 58 % Aortic stenosis, mild, 9.0 Does this patient have ACS? Should he necessarily go to the cath lab? This was done.
She was unable to be defibrillated but was cannulated and placed on ECMO in our Emergency Department (ECLS - extracorporeal life support). After good ECMO flow was established, she was successfully defibrillated. Here is a case of ECMO defibrillation with near shark fin that was due to proximal LAD occlusion. The K was normal.
Angiography : LMCA — 90-99% osteal stenosis. LCx — 50-69% stenosis of the 1st marginal branch; with 100% distal LCx occlusion. He required multiple defibrillations within a period of a few hours. This time, the arrhythmia did not spontaneously terminate — but rather degenerated to VFib, requiring defibrillation.
We administered adrenaline for cardiac excitation, dopamine for maintained blood pressure, sodium bicarbonate to correct the acidosis, and multiple electric defibrillations. Fortunately, there was no obvious stenosis in the right coronary artery.
He was resuscitated with chest compressions and defibrillation and 1 mg of epinephrine. An echocardiogram confirmed aortic stenosis with a large pressure gradient. This young male had ventricular fibrillation during a triathlon. On his bib it stated that he had a congenital heart disorder. His initial ECG is shown here.
The patient had 2 ventricular fibrillation arrests during transport, but was immediately defibrillated both times, and was awake in the ED, when the following ECG was recorded: The ST elevation has mostly resolved on this ECG, and were it not for the arrest and the prehospital ECG, this would not be a slam dunk diagnosis.
Today's case reminds us of the intuitive logic that if a patient has a shockable arrest ( ie, VFib ) — and following successful defibrillation shows evidence of acute OMI ( even if STEMI criteria are not necessarily fulfilled ) — that such patients have much to gain from immediate cath with PCI. ( TIMI-0 flow.
She was found to be in ventricular fibrillation and was defibrillated 8 times without a single, even transient, conversion out of fibrillation. She was immediately intubated during continued compressions, then underwent a 9th defibrillation, which resulted in an organized rhythm at 42 minutes after initial arrest. References : 1.
The arrhythmia spontaneously converted before defibrillation was achieved. Below is a still image with the red arrow indicating the subtotal LMCA stenosis. Just prior to arrival he fell out of consciousness with the below ECG on the monitor. ECG #3 The above ECG shows a polymorphic VT at a rate of about 180 BPM.
She was defibrillated and resuscitated. 1-4 Surprisingly, serial angiographic studies have revealed that the plaque at the site of the culprit lesion of a future acute myocardial infarction often does not cause stenosis that, as seen on the antecedent angiogram, is sufficiently severe to limit flow. Learning Points: 1.
During angiogram in the cath lab, the patient suffered two episodes of ventricular fibrillation for which he was successfully defibrillated. Angiogram showed a culprit lesion of 100% stenosis to the right coronary artery and 100% stenosis of the right posterior descending artery, both with TIMI 0 flow.
The Y descent is shallow in tricuspid stenosis, and absent in cardiac tamponade. 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.
When the ICD was finally interrogated, the syncopal events and shocks correlated with two VF events that were defibrillated successfully. 90% stenosis of the proximal ramus intermedius, pre procedure TIMI II flow The ramus intermedius is a normal variant on coronary anatomy that arises between the LAD and LCX.
We can, therefore, put down the defibrillation pads, set aside the amiodarone, and look further at the ECG. The coronary angiogram revealed no critical stenosis, or acute plaque ulceration. Paradoxically, though, the third green arrow identifies a QRS that is more narrow than the RBBB complexes surrounding it.
He was defibrillated immediately and had return of normal mental status. They found an acute lesion of the LAD at the site of the prior stents, including 70% proximal LAD lesion and 95% mid-LAD stenosis with TIMI 3 flow at the time of cath. In the ambulance during transport, the patient suddenly suffered VF arrest.
In addition, the top left blue arrow indicates a section in the LAD with a severe stenosis, likely the culprit for the prior L A D occlusion which has since recanalized. Rhythm C: This telemetry strip from an older adult was initially thought to need defibrillation. There are also diagonal branches which are not well visualized.
Soon after the witnessed occlusion, the patient suffered ventricular fibrillation arrest, from which he was immediately resuscitated with 1 defibrillation. The note documents that the first view of the LCX showed 99%, TIMI 2 flow, but then (before intervention) was seen to fully occlude in real time (100%, TIMI 0).
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