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He was defibrillated into VT. He then underwent dual sequential defibrillation into asystole. The ECG shows severe ischemia, possibly posterior OMI. But cardiac arrest is a period of near zero flow in the coronary arteries and causes SEVERE ischemia. It takes time for that ischemia to resolve. They started CPR.
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. We found that 38% of out of hospital ventricular fibrillation was due to STEMI.
This certainly looks like an anterior STEMI (proximal LAD occlusion), with STE and hyperacute T-waves (HATW) in V2-V6 and I and aVL. This rules out subendocardial ischemia and is diagnostic of posterior OMI. How do you explain the anterior STEMI(+)OMI immediately after ROSC evolving into posterior OMI 30 minutes later?
You can subscribe for news and early access (via participating in our studies) to the Queen of Hearts here: [link] queen-form This EMS ECG was transmitted to the nearby Emergency Department where it was remotely reviewed by a physician, who interpreted it as normal, or at least without any features of ischemia or STEMI.
This ECG was read as “No STEMI” with no prior available for comparison. It is true this ECG does not meet STEMI criteria (there is 1.0 The patient has also developed sinus bradycardia, which may result from right coronary artery ischemia to the SA node. Instead we discussed 5 minute delays for the STEMI(+) OMI patients.
V1 sits over both the RV and the septum, so transmural ischemia of either one with give OMI pattern in V1 and reciprocal STD in V5 and V6. See this post: Septal STEMI with ST elevation in V1 and V4R, and reciprocal ST depression in V5, V6. She was successfully defibrillated and taken back to the ED. The family sued.
The ECG shows obvious STEMI(+) OMI due to probable proximal LAD occlusion. 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.
He underwent further standard resuscitation EXCEPT that we applied the Inspiratory Threshold Device ( ResQPod ) AND applied Dual Sequential Defibrillation (this simply means we applied 2 sets of pads, had 2 defib machines, and defibrillated with both with only a fraction of one second separating each defibrillation.
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.
Here is his ED ECG: There is obvious infero-posterior STEMI. What are you worried about in addition to his STEMI? 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. There is atrial fibrillation.
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).
None of these findings are diagnostic of ischemia, but they should give you a high index of suspicion and prompt serial ECGs at a minimum. He was defibrillated. Anterolateral STEMI. Ischemia comes and goes. mm of STE at 60 ms after the J-point in lead V3, 400 ms QTc, and 6 mm of R-wave amplitude in V4.
She was never seen to be in ventricular fibrillation and was never defibrillated. This ECG is diagnostic of diffuse subendocardial ischemia. Note that they finally have laid to rest the new or presumably new LBBB as a criteria for STEMI. Also note that they allow ST depression c/w posterior MI to be a STEMI equivalent.
If it is STEMI, it would have to be RBBB with STEMI. Followup ECG: No Change Absence of evolution is the best evidence against ischemia as the etiology. I was taught that the tell-tale sign of ischemia vs an electrical abnormality was in the hx, i.e. chest pain for the ischemia and potential syncope for brugada.
It could at least say: "ST Elevation, consistent with normal variant," or "consistent with ischemia or normal variant," or "consistent with early repolarization." So there is definitely no STEMI, and the STE is normal. But after reading this blog, you all know that most OMI do NOT meet STEMI criteria. mm in men over age 40.
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. There is a very small amount of STE in some of the anterior, lateral, and inferior leads which do NOT meet STEMI criteria. Here is his ECG on arrival: What do you think?
After the second defibrillation the patient had an organized rhythm: Bradycardic escape/agonal rhythm, with large ST deviations. A repeat ECG was done: Obvious anterolateral wall STEMI. It should have been shocked at least 10 seconds ago. Beats 4, 6, and 7 are narrow, as the rhythm is trying to resume from above the ventricles.
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.
She was defibrillated and resuscitated. STEMI MINOCA versus NSTEMI MINOCA STEMI occurs in the presence of transmural ischaemia due to transient or persistent complete occlusion of the infarct-related coronary artery. This has resulted in an under-representation of STEMI MINOCA patients in the literature. From Gue at al.
2) The STE in V1 and V2 has an R'-wave and downsloping ST segments, very atypical for STEMI. Cardiology was consulted and they agreed that the EKG had an atypical morphology for STEMI and did not activate the cath lab. Smith comment: 1) Brugada ECG may have ST shifts in limb leads as well as precordial leads. Bicarb 20, Lactate 4.2,
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.
After epinephrine, atropine, and defibrillation x 2, there was a return of pulses. There is ST depression in II, III, and aVF that is concerning for reciprocal depression from high lateral STEMI in aVL, where there is some ST elevation. However, with widespread ST depression, this could also be due to diffuse subendocardial ischemia.
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.
A 12-lead was recorded, showing "STEMI," but is unavailable. Moreover, if you know that catastrophic intracranial hemorrhage can result in an ECG that mimics STEMI, then you know that this patient probably has a severe intracranial hemorrhage. She was BVM ventilated and suctioned. Shortly thereafter, pulses were lost.
Unfortunately, the ECG was interpreted as no significant change from prior , "no STEMI"!! Defibrillation was performed, and ROSC was achieved. Approximately 5 minutes after ROSC, this ECG was obtained (about 45 minutes after arrival): Obvious anterolateral OMI, and STEMI criteria positive for those who care or need it.
It is possible there is microvascular dysfunction producing residual transmural ischemia. But this is most common when there is prolonged ischemia, and this patient had the fastest reperfusion imaginable! She was defibrillated perhaps 25 times. Defibrillation strategies for refractory ventricular fibrillation. McLeod, S.
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