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Bedside cardiac ultrasound showed moderately decreased LV function. 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. She was intubated.
He required multiple defibrillations within a period of a few hours. There is no definite evidence of acute ischemia. (ie, This time, the arrhythmia did not spontaneously terminate — but rather degenerated to VFib, requiring defibrillation. Some residual ischemia in the infarct border might still be present.
It was reportedly a PEA arrest; there was no recorded V Fib and no defibrillation. In terms of ischemia, there is both a signal of subendocardial ischemia (STD max in V5-V6 with reciprocal STE in aVR) AND a signal of transmural infarction of the inferior wall with Q wave and STE in lead III with reciprocal STD in I and aVL.
This case was provided by Spencer Schwartz, an outstanding paramedic at Hennepin EMS who is on Hennepin EMS's specialized "P3" team, a team that receives extra training in advanced procedures such as RSI, thoracostomy, vasopressors, and prehospital ultrasound. She was defibrillated and resuscitated. It can only be seen by IVUS.
Ischemic ST-Segment Depression Maximal in V1-V4 (Versus V5-V6) of Any Amplitude Is Specific for Occlusion Myocardial Infarction (Versus Nonocclusive Ischemia). When the ICD was finally interrogated, the syncopal events and shocks correlated with two VF events that were defibrillated successfully. J Am Heart Assoc. doi: 10.1161/JAHA.121.022866.
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 was managed medically with Clopidogrel.
Her bedside cardiac ultrasound was normal We decided to cardiovert her since the time of onset was very recent. But when you see this, you should suspect that the AV node is not well. Our electrophysiologist told me that highly trained athletes can have such high vagal tone that they do not have a rapid ventricular response.
After epinephrine, atropine, and defibrillation x 2, there was a return of pulses. 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?
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