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15 minutes after EMS arrival, after at least 6 defibrillations, the patient achieved sustained ROSC. Despite anticipation by many that the initial post-resuscitation ECG will show an obvious acute infarction — this expected "STEMI picture" is often not seen. Meyers and Smith in the October 15, 2022 post of Dr. Smith's ECG Blog ).
A patient had a cardiac arrest with ventricular fibrillation and was successfully defibrillated. COACT: The COACT trial was fatally flawed, and because of it, many cardiologists are convinced that if there are no STEMI criteria, the patient does not need to go to the cath lab. Lemkes JS, Janssens GN, van der Hoeven NW, et al.
He was defibrillated into VT. He then underwent dual sequential defibrillation into asystole. See these related cases: Cardiac arrest, defibrillated, diffuse ST depression and ST Elevation in aVR. Cardiac arrest #3: ST depression, Is it STEMI? This patient was witnessed by bystanders to collapse. They started CPR.
The ECG shows obvious STEMI(+) OMI due to probable proximal LAD 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. The below ECG was recorded. What do you think?
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.
Again, it is common to have an ECG that shows apparent subendocardial ischemia after resuscitation from cardiac arrest, after defibrillation, and after cardioversion. We found that 38% of out of hospital ventricular fibrillation was due to STEMI. Much depends on the post resuscitation ECG and its evolution shortly after defibrillation.
He reports that this chest pain feels different than prior chest pain when he had his STEMI/OMI, but is unable to further describe chest pain. VF was refractory to amiodarone, lidocaine, double-sequential defibrillation, esmolol, etc. Sensitivity was 87% for OMI in our validation study (it was 34% for STEMI criteria).
This certainly looks like an anterior STEMI (proximal LAD occlusion), with STE and hyperacute T-waves (HATW) in V2-V6 and I and aVL. How do you explain the anterior STEMI(+)OMI immediately after ROSC evolving into posterior OMI 30 minutes later? This caused a type 2 anterior STEMI.
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.
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. They also sued both EMTs for allegedly not starting chest compressions and defibrillating quickly enough. Also seen in inferior + RV OMI.) There is also STD in V2.
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.
Are Some Cardiologists Really Limited by Strict Adherence to STEMI millimeter criteria? He was found in ventricular fibrillation and defibrillated, then brought to a local ED which does not have a cath lab. This is the response he got: Interventionist: "No STEMI, no cath. It is a STEMI equivalent.
There’s inferior ST depression which is reciprocal to subtle lateral convex ST elevation, and the precordial T waves are subtly hyperacute – all concerning for STEMI(-)OMI of proximal LAD. There’s ST elevation I/aVL/V2 that meet STEMI criteria. This is obvious STEMI(+)OMI of proximal LAD. Non-STEMI or STEMI(-)OMI?
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 Queen of Hearts sees it of course: Still none of these three ECGs meet STEMI criteria. Do you think we discussed this patient's 2-3 hour delay to reperfusion in our quarterly "STEMI meeting"?
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.
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. Bedside echo revealed anteroseptal wall motion abnormality at which point I activated a code STEMI. Defibrillated out of v fib in the cath lab. mm in men over age 40.
He was resuscitated with chest compressions and defibrillation and 1 mg of epinephrine. Thus, this patient had increased ST elevation (current of injury) superimposed on the ST elevation of LVH and simulating STEMI. This young male had ventricular fibrillation during a triathlon. His initial ECG is shown here. He awoke and did well.
Discharge ECG showed antero-inferior reperfusion T wave inversion: Had the initial ECG been signed off as “STEMI negative” the patient could have arrested in the waiting room, with a poor cardiac and neurological outcome. For more on this topic — See discussion in the October 24, 2019 and July 31, 2018 posts in Dr. Smith's ECG Blog ).
RBBB in acute STEMI has a very high mortality. But here there is a large degree of ST elevation in V2-V6, I, and aVL. The paramedics activated the cath lab from the field.
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).
He was defibrillated. Anterolateral STEMI. The formula results in 23.43, just above the 23.4 The patient was diagnosed with esophageal reflux and was being discharged by the nurse when he had a cardiac arrest. Here is his post resuscitation ECG: Now the diagnosis is obvious.
There is a very small amount of STE in some of the anterior, lateral, and inferior leads which do NOT meet STEMI criteria. The case was reviewed by all parties, and it was stated correctly that the ECG does not meet the STEMI criteria. He was defibrillated immediately and had return of normal mental status.
She was never seen to be in ventricular fibrillation and was never defibrillated. Note that they finally have laid to rest the new or presumably new LBBB as a criteria for STEMI. Note that they finally have laid to rest the new or presumably new LBBB as a criteria for STEMI. BP gradually rose. Kurkciyan et al.
This is another case written by Pendell Meyers (who is helping to edit the blog and has many great recent posts) Case A 45 year old man was driving to work when he experienced acute onset sharp left sided chest pain with paresthesias of the left arm. A repeat ECG was done: Obvious anterolateral wall STEMI.
If it is STEMI, it would have to be RBBB with STEMI. Cardioversion/defibrillation. But — one of the causes of Brugada Phenocopy is acute infarction — so I didn’t know how to distinguish between a preexisting Brugada-1 ECG pattern vs a Brugada ECG pattern developing as a result of acute ongoing anterior STEMI. Hypothermia.
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.
When the ICD was finally interrogated, the syncopal events and shocks correlated with two VF events that were defibrillated successfully. Recall that air is a poor conductor of electricity and will, therefore, generate smaller amplitudes on posterior leads (hence why STEMI criteria requires only >0.5
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,
It was reportedly a PEA arrest; there was no recorded V Fib and no defibrillation. NOTE: For more on the ECG diagnosis of acute RV "strain" ( and acute PE ) — Please check out My Comment at the bottom of the page in the March 28, 2022 post in Dr. Smith's ECG Blog. CPR was initiated immediately.
to greatly decrease risk (although in STEMI, the optimal level is about 4.0-4.5 Here are other posts on hyperK, large calcium doses for hyperK, and ventricular tachycardia in hyperK Weakness, prolonged PR interval, wide complex, ventricular tachycardia Very Wide and Very Fast, What is it? How would you treat? If the patient is at 1.8,
The computer called this Acute STEMI What do you think? STEMI never has a very short QT. There is Bazett, Fridericia, Hodges, Framingham and Rautaharju -- see here at mdcalc: [link] If the ST Elevation here were due to STEMI, it would be an LAD Occlusion. Treatment is by ICD ( implantable cardioverter defibrillator ).
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. She collapsed and 911 was called; she was found pulseless. Exact rhythm during arrest is uncertain.
How well does the computer interpretation perform? -- in this case, the computer diagnosed STEMI but the patient had Fever with Brugada _ _ Fever and Brugada-- Important articles The literature below shows that fever-induced Brugada is indeed a high risk for an arrhythmic event. Syncope and ST Segment Elevation. And another finding.
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.
Soon after the witnessed occlusion, the patient suffered ventricular fibrillation arrest, from which he was immediately resuscitated with 1 defibrillation. Final Diagnosis: "STEMI" (of course, as you can see in the ECGs above, this is not true, by definition this was NSTEMI. In other words, millimeters really don't matter!
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.
Several 200 J shocks did not terminate the VF, so a second defibrillator was applied for double sequential defibrillation with 400 J. She was defibrillated perhaps 25 times. Propranolol versus Metoprolol for treatment of electrical storm in patients with implantable cardioverter-defibrillator. SanzRuiz, R., Solis, J., &
Queen : she saw no OMI (no "STEMI Equivalent") either Continued : Now, she says she was walking to the bathroom when she experienced acute onset substernal chest pressure radiating into her neck and left arm. Throughout this process, the patient had repeated VF and was defibrillated 8 times. It is almost certainly not acute.
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