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Delayed First Medical Contact to Reperfusion Time Increases Mortality in Rural EMS Patients with STEMI. Delayed First Medical Contact to Reperfusion Time Increases Mortality in Rural EMS Patients with STEMI. We looked at 101 STEMI patients from two rural EDs. Date: November 22, 2023 Reference: Stopyra et al.
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 paramedic called the EM physician ahead of arrival and discussed the case and ECGs, and both agreed upon activating "Code STEMI" (even though of course it is not STEMI by definition), so that the acute LAD occlusion could be treated as fast as possible. So the cath lab was activated. Long term outcome is unavailable.
Interpretation : diagnostic of acute anterior OMI with STE less than STEMI criteria in V1-V4, hyperacute T waves in V2-V4, and suspiciously flat isoelectric ST segments in III and aVF suspicious for reciprocal findings. Now it even meets STEMI criteria, and HATWs continue to inflate. So the cath lab was not activated. Ongoing OMI.
While in the ED, patient developed acute dyspnea while at rest, initially not associated with chest pain. The patient had no chest symptoms until he had been in the ED for many hours and had been undergoing management of his DKA. The patient was under the care of another ED physician. Another ECG was recorded: What do you think?
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.
If it looks and feels like a STEMI clinically, get serial ECGs and consult Cardiology immediately. If it looks and feels like a STEMI clinically, get serial ECGs and consult Cardiology immediately. Take Home Points Provider assessment of how the patient looks is extremely important.
He arrived to the ED with severe hypotension, heart rate in the 70s, unable to follow commands but moving all extremities requiring restraint and sedation, respiratory rate around 24/min being supported with bag valve mask, with significant hypoxemia. His family started CPR and called EMS, who arrived to find him in ventricular fibrillation.
The ST changes went overlooked by both the ED physician and the on-call cardiologist, and the patient was subsequently admitted to telemetry. it has been subsequently deemed a STEMI-equivalent. These sunken J-points make a rapid, crescendo rise into large, fat, and bulky T waves. However, when the Troponin I returned 8.4
A prehospital “STEMI” activation was called on a 75 year old male ( Patient 1 ) with a history of hyperlipidemia and LAD and Cx OMI with stent placement. He arrived to the ED by helicopter at 1507, about three hours after the start of his chest pain while chopping wood around noon. He wrote most of it and I (Smith) edited.
The interventional cardiologist then canceled the activation and returned the patient to the ED without doing an angiogram ("Not a STEMI"). Despite the ACC guidelines for posterior STEMI, the cardiologist again refused to take the patient to the cath lab. mm STE in the posterior leads.
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. See these posts: Chest Pain, ST Elevation, and an Elevated Troponin: Should we Activate the Cath Lab?
Our data corroborate that immediate management of a patient with a normal automated triage ECG reading is not modified by real-time ED physician ECG interpretation." Smith comment: we showed that the first troponin, even in full-blown STEMI, is negative 25% of the time. But according to Langlois-Carbonneau et al.,
The biggest problem with STEMI criteria are false negatives – because this costs patient’s myocardium, with greater mortality and morbidity. The essential "immediate" decision to be made in "zero time" in the ED, is whether or not prompt cath and reperfusion is needed. Could this false positive cath lab activation been prevented?
An undergraduate (not yet in medical school) who works as an ED technician (records all EKGs, helps with procedures, takes vital signs) and who reads this blog regularly arrived at work and happened to glance down and see this previously recorded ECG on a table in the ED. The young ED tech immediately suspected LAD OMI.
This was sent by an undergraduate (not yet in medical school, but applying now) who works as an ED technician (records all EKGs, helps with procedures, takes vital signs) and who reads this blog regularly. The patient re-presented to the ED a few days after his discharge with syncope. Edited by Smith He also sent me this great case.
While STEMI negative, the ECG is diagnostic of proximal LAD occlusion. It’s unclear if the paramedic ECGs were seen or missed in the ED. Transient STEMI” are often managed like non-STEMI with delayed angiography, which is very risky. At this point the emergency physician asked for a stat cardiology consult.
This ECG was texted to me with the implied question "Is this a STEMI?": I responded that it is unlikely to be a STEMI. Septal STEMI often has ST depression in V5, V6, reciprocal to V1. Then combine with clinical presentation and low pretest probability 2 Saddleback STEMIs A Very Subtle LAD Occlusion.T-wave wave in V1??
He arrived initially with diaphoresis and pallor which have self-resolved following arrival to the ED. Serial ECG's should be obtained to assess for evolution to acute STEMI. As demonstrated by this case, serial EKG’s may show complete resolution of these findings without progressing into a STEMI pattern.
Methods and Results Patients with confirmed ST elevation myocardial infarction (STEMI) treated by emergency medical services were included in this retrospective cohort analysis of the AVOID study. Having severe pain drives people to the ED for faster treatment! We analyzed 1409 STEMI activations (69% male, 66.3 years old ± 13.7
4,5] We have now formally studied this question: Emergency department Code STEMI patients with initial electrocardiogram labeled ‘normal’ by computer interpretation: a 7-year retrospective review.[6] have published a number of warnings about the previous reassuring studies.[4,5]
With a new protocol and Pulsara, Metropolitan Emergency Medical Services can now transport eligible pediatric behavioral health patients directly to behavioral health facilities—resulting in a 44% decrease of pediatric behavioral health patients transported to the ED. MEMS transports around 77,000 patients each year.
This study shows that for a transient STEMI ("complete normalization of ST segments"), it is not unequivocally necessary to activate the cath lab emergently. This might extend to Wellens' syndrome, which is really and transient STEMI in which the ST Elevation is not recorded. See more cases of Transient STEMI here: [link]
Both cases had an EMS ECG that was transmitted to the ED physician asking "should we activate the cath lab?" Here they are: Patient 1, ECG1: Zoll computer algorithm stated: " STEMI , Anterior Infarct" Patient 2, ECG1: Zoll computer algorithm stated: "ST elevation, probably benign early repolarization." What do you think?
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."
He had walked into the ED (did not use EMS). 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. Exact pain history was difficult to ascertain. There was some SOB. Could it be acute (vs.
On ED arrival GCS is 3, there are rapid eye movements to the right but no other apparent seizure activity. Official diagnosis requires EEG, which is not something we can typically obtain in the ED. This document covers high sensitivity troponin, risk disposition pathways, and STEMI equivalents.
He called EMS who brought him to the ED. She knows the baseline is normal, and she knows the STEMI(-) OMI one is diagnostic of OMI, with the highest possible confidence. Here is the EM decision making: "The patient's EKG revealed some repolarization abnormalities but no clear signs of a STEMI. ED Diagnoses: 1.
Jason was very skeptical of STEMI. This also argues against STEMI. Unfortunately, this option might not be available for pre-hospital tracings ( but it can be done once the patient arrives in the ED for their initial hospital tracing ). He complained of 3 days of diarrhea and abdominal pain. What do you think? Jason, I agree.
A male in his 40's who had been discharged 6 hours prior after stenting of an inferoposterior STEMI had sudden severe SOB at home 2 hours prior to calling 911. The patient was transported to the ED. Here is his ED ECG: There is sinus tachycardia. Is this acute STEMI? Is this an acute STEMI? -- Unlikely!
Here is his initial ED ECG: What do you think? Here it is: Obvious Inferior Posterior STEMI (+) OMI. Then the ED doc would be dependent on that first ECG. Initial troponin was: 3 ng/L We showed that the first troponin in acute STEMI is often negative in at least 27%. Or had not had a prehospital ECG on the ambulance.
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?
The attending crews were concerned for SVT with corresponding ischemic hyperacute T waves (HATW) and subsequently activated STEMI pre-hospital. The following ECG was captured upon arrival at the receiving ED. The ED resulted an 8.7 Then, three minutes later… Crews activated STEMI as she deteriorated into PEA arrest.
A 61 year-old with chest pain arrived to the ED by ambulance with resolving chest pain. Here is his ED ECG: The computer interpretation was " normal " What do you think? The cath lab was activated, as it should be with transient STEMI. This ECG is NOT normal. The T-waves in V2-V4 are very large in proportion to the QRS.
It is unclear what changes happened to the rhythm based on the EMS interventions, but the patient arrived to the ED remaining critically ill and with a very wide complex reported (no ECGs from ED available sadly). Hyperkalemia was diagnosed and more treatment was given including more calcium, bicarb, insulin/dextrose, and albuterol.
Here was his initial ED ECG: Formal interpretation by interventional cardiologist: There is "Non-diagnostic" ST Elevation in V2-V4 and aVL. 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.
He had walked into the ED (did not use EMS). 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. Exact pain history was difficult to ascertain. There was some SOB.
Self-medicated with 600 mg Ibuprofen and 750 mg Paracetamol (no change) prior to driving to the ED. See my formula for differentiating anterior LV aneurysm (that is to say, persistent ST elevation after old MI) from acute anterior STEMI. Both support acute anterior STEMI. BP 112/80, SpO2 100%. Unremarkable physical examination.
Sent by anonymous, written by Pendell Meyers, reviewed by Smith and Grauer A man in his 40s presented to the ED with HTN, DM, and smoking history for evaluation of acute chest pain. In the available view of the sinus rhythm, we see normal variant STE which probably meets STEMI criteria in V4 and V5. Triage ECG: What do you think?
This worried the crew of potential acute coronary syndrome and STEMI was activated pre-hospital. Below is the initial ED ECG. As it currently stands, an ST/S ratio >15% should raise awareness for new anterior STEMI. Manual of Cardiovascular Medicine (5th ed.). Smith comment : V5 and V6 are excessively discordant!!!!
A 36 yo male smoker presented to the ED with chest pain. 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. See more on STE in aVR in anterior STEMI, below.
He is interested and experienced in healthcare informatics, previously worked with ED-directed EMR design, and is involved in the New York City Health and Hospitals Healthcare Administration Scholars Program (HASP). She arrives in the emergency department (ED) with decreased level of consciousness and shock.
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