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Again, it is common to have an ECG that shows apparent subendocardial ischemia after resuscitation from cardiac arrest, after defibrillation, and after cardioversion. and repeat the ECG, to see if the apparent ischemia persists. The estimated left ventricular ejection fraction is 58 % Aortic stenosis, mild, 9.0
He was resuscitated with chest compressions and defibrillation and 1 mg of epinephrine. ACS would be highly unusual in a young athlete, and given the information on his race bib, one must first suspect that the abnormal ST elevation is due to demand ischemia, not ACS. This young male had ventricular fibrillation during a triathlon.
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 rules out subendocardial ischemia and is diagnostic of posterior OMI. V4-5 continue to show STD. 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. see below).
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.
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.
The first task when assessing a wide complex QRS for ischemia is to identify the end of the QRS. The ST segment changes are compatible with severe subendocardial ischemia which can be caused by type I MI from ACS or potentially from type II MI (non-obstructive coronary artery disease with supply/demand mismatch). What do you think?
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. There is no definite evidence of acute ischemia. (ie, Some residual ischemia in the infarct border might still be present.
The patient has also developed sinus bradycardia, which may result from right coronary artery ischemia to the SA node. During angiogram in the cath lab, the patient suffered two episodes of ventricular fibrillation for which he was successfully defibrillated. Two stents were placed with resultant TIMI 3 flow.
This ECG is all but diagnostic of subepicardial ischemia of the anterior, lateral, and inferior walls, most likely due to Occlusion MI (OMI), probably of the LAD. He was defibrillated immediately and had return of normal mental status. Here is his ECG on arrival: What do you think? Leads II and aVF also have hyperacute T-waves.
The ECG shows sinus rhythm with normal QRS complex morphology and significant subendocardial ischemia (SEI) pattern (ST depression in many leads, worst in lateral areas including leads II, V5-6, with reciprocal STE in aVR). Here is her ECG within 30 minutes of PCI: Improved, but still with ischemia. Pre-intervention. Post-intervention.
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