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Date: November 22, 2023 Reference: Stopyra et al. Delayed First Medical Contact to Reperfusion Time Increases Mortality in Rural EMS Patients with STEMI. Date: November 22, 2023 Reference: Stopyra et al. Delayed First Medical Contact to Reperfusion Time Increases Mortality in Rural EMS Patients with STEMI.
Background: Primary PCI is the recommended reperfusion strategy in patients with STEMI and should be initiated within 2 hours after first medical contact. Paper: Van de Werf, F et al. In non-PCI-capable hospitals this goal is not always achievable due to delays in transfer. Primary PCI: 95.7% Primary PCI: 95.7% Primary PCI: 78.4%
A 60 yo with 2 previous inferior (RCA) STEMIs, stented, called 911 for one hour of chest pain. Here is his most recent previous ECG: This was recorded after intervention for inferior STEMI (with massive ST Elevation, see below), and shows inferior Q-waves with T-wave inversion typical of completed inferior OMI. ng/mL (quite large).
The ECG did not meet STEMI criteria, and the final cardiology interpretation was “ST and T wave abnormality, consider anterior ischemia”. There’s only minimal ST elevation in III, which does not meet STEMI criteria of 1mm in two contiguous leads. But STEMI criteria is only 43% sensitive for OMI.[1]
I sent this to the Queen of Hearts So the ECG is both STEMI negative and has no subtle diagnostic signs of occlusion. Non-STEMI guidelines call for “urgent/immediate invasive strategy is indicated in patients with NSTE-ACS who have refractory angina or hemodynamic or electrical instability,” regardless of ECG findings.[1]
So while there’s no diagnostic STEMI criteria, there are multiple ischemic abnormalities in 11/12 leads involving QRS, ST and T waves, which are diagnostic of a proximal LAD occlusion. First trop was 7,000ng/L (normal 25% of ‘Non-STEMI’ patients with delayed angiography have the exact same pathology of acute coronary occlusion.
Cath lab declined as it is not a STEMI." And now this finding is even formally endorsed as a "STEMI equivalent" in the 2022 ACC guidelines!!! Another myocardial wall is sacrificed at the altar of the STEMI/NonSTEMI mindset. de Winter et al in N Engl J Med 359:2071-2073, 2008. Cath attending is aware. Abstract 556.
Now lets walk through them quickly: Ho et al (4) looked at termination of VT in 15 min or hemodynamic deterioration. Gorgels et al (5) looked at procainamide vs lidocaine and again and primary outcome was VTach termination. Manz et al (6) looked at ajmaline vs lidocaine for the termination of VT. and Komura et al.,
The latest is Langlois-Carbonneau et al. If we took this as the gold standard, we would conclude that the computer interpretation was safe and accurate at least accurate enough to not miss STEMI, and that physicians should not be interrupted to interpret it, because there would be no change in patient management.
They wanted to know if I would like them to activate the outside hospital's "STEMI alert." But of course, this is not a STEMI by definition as it does not meet STEMI criteria. The STEMI guidelines do state that hyperacute T-waves "may indicate early acute myocardial infarction" but do not discuss it as a "STEMI equivalent."
Many conditions outside of acute coronary syndrome (ACS) mimic ST-elevation myocardial infarction (STEMI), but only a handful of cases have reported ST-elevations (STE) in the setting of pancreatic inflammation where underlying ACS was excluded. 2 Proposed hypothesis as described by Hsu et al., Yu ES, Lange JJ, Broor A, et al.
Date: September 8th, 2021 Reference: Desch et al. Date: September 8th, 2021 Reference: Desch et al. Defibrillation is the treatment of choice in these cases but does not often result in sustained ROSC ( Kudenchuk et al 2006). The TOMAHAWK Investigators. first appeared on The Skeptics Guide to Emergency Medicine.
[display_podcast] Date: October 19th, 2017 Reference: Hofmann et al. display_podcast] Date: October 19th, 2017 Reference: Hofmann et al. The ECG shows an inferior ST-Elevated Myocardial Infarction (STEMI). A systematic review by Wijesinge et al from 2009 found only two randomized control trials looking at supplemental oxygen.
This was a machine read STEMI positive OMI. 118.007305) from Heitner et al. , The meaning of this quote is that at times, something as obvious as the dramatic anterior lead ST elevation that we see in today's tracing is not the result of an acute LAD STEMI. His ECG is shown below. Pretty obvious anterior current of injury.
So this NSTEMI was likely a STEMI(-)OMI with delayed reperfusion. The patient was admitted as ‘NSTEMI’ which is supposed to represent a non-occlusive MI, but the underlying pathophysiology is analogous to a transient STEMI. Deutch et al. Fortunately the patient did not reocclude while awaiting the angiogram.
Microaxial Flow Pump or Standard Care in Infarct-Related Cardiogenic Shock Møller JE et al. DOI: 10.1056/NEJMoa2312572 Clinical Question In adults presenting with STEMI and cardiogenic shock does the use of a microaxial flow pump (Impella CP) compared to standard care reduce death from any cause at day 180?
BP 142/100 HR 90 RR 16 (BBS CTA) SpO2 99 (RA) Dstick 110 My colleagues noted the ST-depression in the respective leads, as well, and STEMI activated to the nearest PCI center. 1] Here is the admitting ED ECG after cancellation of Code STEMI. The EMS crews were correct moving forward with STEMI activation. 1] Driver, B.
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. These physicians did not want a patient with an OMI that was not a STEMI to be randomized to no angiogram.
Their OMI Manifesto details how use of standard STEMI criteria results in an unacceptable level of inaccuracy, in which an estimated 25-30% of acute coronary occlusions are missed! The article by Aslanger, Smith et al that is featured above in today’s post has just been published.
Thus, this is both an anterior and inferior STEMI. How old is this antero-inferior STEMI? Although acute anterior STEMI frequently has narrow QR-waves within one hour of onset (1. Raitt et al.) [and Armstrong et al.)], the presence of such well developed anterior Q-wave suggests completed transmural STEMI.
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?
Smith’s ECG Blog has published a growing list of over 40 cases of ECGs falsely labeled ‘normal’ by the computer which are diagnostic of Occlusion MI, and Smith et al. This is diagnostic of LAD occlusion but is equivocal for STEMI criteria and was missed (and both labeled ‘normal’ by final cardiology interpretation).
You can see how V1, V2, aVR, and V4R would have ST elevation in either a right ventricular STEMI or with a septal STEMI, and how lateral leads, and even posterior leads, would have reciprocal ST depression. In a 1999 study by Engelen et al. of patients with anterior STEMI, ST elevation of greater than or equal to 3.0
Date: January 28th, 2019 Reference: Chu DK et al. Date: January 28th, 2019 Reference: Chu DK et al. In the 2015 AVOID study there was some suggestion of increased MI size in the group of STEMI patients that received oxygen at 8 L/min compared to a room air control group. Reference: Chu DK et al. The Lancet 2018.
Lindahl et al. From Gue at al. 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. References: 1.
Thus, this is BOTH an anterior and inferior STEMI in the setting of RBBB. How old is this antero-inferior STEMI? Although acute anterior STEMI frequently has narrow QR-waves within one hour of onset (1. Raitt et al.), Raitt et al.), Armstrong et al.), 3) Oliva et al. (4) Armstrong PW et al.
link] Hughes KE et al. The cath lab was activated, as it should be with transient STEMI. See this case of transient STEMI: Spontaneous Reperfusion and Re-occlusion - My Bad Thinking Contributes to a Death. Computer algorithms are completely unreliable at diagnosing STEMI, with both poor sensitivity and poor specificity.
Date: February 1, 2023 Reference: Wolfrum et al. Date: February 1, 2023 Reference: Wolfrum et al. A post-arrest ECG doesn’t show any signs of STEMI. Temperature Control After In-Hospital Cardiac Arrest: A Randomized Clinical Trial. Circulation. first appeared on The Skeptics Guide to Emergency Medicine. Circulation.
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 worried the crew of potential acute coronary syndrome and STEMI was activated pre-hospital. As it currently stands, an ST/S ratio >15% should raise awareness for new anterior STEMI. Smith comment : V5 and V6 are excessively discordant!!!! Here are two examples of HATW’s in the setting of confirmed LVH. Josephson, M. 40; 1234-1241.
A prehospital STEMI activation was transmitted to the closest PCI center, and 324mg ASA was administered. The attending crews were concerned for an ACS-equivalent of LAD occlusion and initiated a prehospital STEMI activation to the closest PCI center. As the conversation progressed, another ECG spontaneously printed. 2] Driver, B.
Echo on the day after admission showed EF of 30-35% and antero-apical wall akinesis with an LV thrombus [these frequently form in complete or near complete (no early reperfusion) anterior STEMI because of akinesis/stasis] 2 more days later, this was recorded: ST elevation is still present. Claeys MJ, Bosmans J, Veenstra L, et al.
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 Armstrong et al. The Queen of Hearts sees it of course: Still none of these three ECGs meet STEMI criteria. Instead we discussed 5 minute delays for the STEMI(+) OMI patients.
This is diagnostic of infero-posterior OMI, but it is falsely negative by STEMI criteria and with falsely negative posterior leads (though they do show mild ST elevation in V4R). They were less likely to have STEMI on ECG, and more likely to be initially diagnosed as non-ACS. Herzog et al. Khan et al. Circulation 2007 2.
The receiving emergency physician consulted with interventional cardiology who stated there was no STEMI. Bigger et al. Is there STEMI? Sadowski ZP, Alexander JH, Skrabucha B, et al. Am Heart J 1999;137: 792–8 Alexander JH, Granger CB, Sadowski Z, et al, for the GUSTO-I and GUSTO-IIb Investigators. Leave it alone.
The attending crews were concerned for SVT with corresponding ischemic hyperacute T waves (HATW) and subsequently activated STEMI pre-hospital. Then, three minutes later… Crews activated STEMI as she deteriorated into PEA arrest. A finger-stick glucose resulted 551 mg/dL, and the following ECG was recorded. 2] Birnbaum, Y., Physiology.
The prehospital and ED computer interpretation was inferior STEMI: There’s normal sinus rhythm, first degree AV block and RBBB, normal axis and normal voltages. The paramedic notes called STEMI into question: “EMS disagree with monitor for STEMI callout. Vitals were normal except for oxygen saturation of 94%. Vitals were normal.
Notice on the right side of the image how the algorithm correctly measures STE sufficient in V1 and V2 to meet STEMI criteria in a man older than age 40. As most would agree, this ECG shows highly specific findings of anterolateral OMI, even with STEMI criteria in this case. Thus, this is obvious STEMI(+) OMI until proven otherwise.
The conventional machine algorithm interpreted this ECG as STEMI. See this post of RV MI with both McConnell sign and "D" sign: Inferior and Posterior STEMI. She was out walking her dog when she developed sudden dizziness and light-headedness. When EMS found her, she was dyspneic and diaphoretic.
Here it is: Obvious Inferior Posterior STEMI (+) OMI. Initial troponin was: 3 ng/L We showed that the first troponin in acute STEMI is often negative in at least 27%. Aside on ECG Research: 20% of Definite diagnostic STEMI (Cox et al.) The cath lab was activated prehospital But imagine if the patient had walked in.
for those of you who do not do Emergency Medicine, ECGs are handed to us without any clinical context) The ECG was read simply as "No STEMI." In fact, Kosuge et al. Stein et al. This is a paper worth reading : Marchik et al. Kosuge et al. Witting et al. of patients with PE and 3.3% of patients without PE.
The criteria of Armstrong et al. would require the ST/S ratio to be 25% for diagnosis of STEMI in LVH. The physician was concerned about STEMI, but also worried that she was overreacting, with the potential that LVH was producing a "STEMI-mimic." Can you diagnose an ACO (STEMI) when you also have LVH? J Emerg Med.
The Queen of Hearts agrees: Here the Queen explains why: However, it was not interpreted correctly by the providers: ED interpretation of ECG: "paced rhythm, LBBB but no STEMI pattern." Most large STEMI have peak troponin I in the 20.0 There are hyperacute T-waves in V5 and V6. Next trop in AM. Peak trop 257.97 ng/mL - 80.0
Quiz : What percent of full blown STEMI have an open artery with normal flow at angiogram? It too is "normal" and you decide that this is not OMI or STEMI and you just decide to get troponins. Jesse McLaren et al. I would expect that a stent would be placed. In the meantime, a lot of myocardium is lost.
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