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And for STEMI too. The post JJ 16 Heparin for ACS and STEMI appeared first on Emergency Medicine Cases. We’re expected to routinely give heparin for all these NSTEMI and unstable angina patients with any ischemic changes seen on the ECG, right? But should we?
Written by Pendell Meyers A man in his 40s called EMS for acute chest pain that awoke him from sleep, along with nausea and shortness of breath. Because the most severe LAD OMIs can cause ischemic failure of the RBB and LAF, any patient with ACS symptoms and new RBBB and LAFB with any concordant STE has LAD OMI until proven otherwise.
The post EM Quick Hits 50 Normal Unenhanced CT Renal Colic DDx, Perichondritis, Magnesium in Pediatric Asthma, Steroids for Pneumonia, OMI Cath Lab Activation appeared first on Emergency Medicine Cases.
According to the EMS narrative, this patient initially refused hospital transport and advised that he would seek evaluation at a later time with his personal physician. A prehospital STEMI activation was transmitted to the closest PCI center, and 324mg ASA was administered. It’s important to stress the presence of a normal QRS (i.e.,
Based on recent studies, current guidelines recommend that O2 should not be given to non-hypoxemic patients with STEMI or NSTEMI [2,3]. REBEL Cast Ep114 – High Flow O2, Suspected ACS, and Mortality? 4159 patients (10% of total population) had STEMI 30d Mortality: High O2 protocol: 8.8% Low O2 protocol: 3.1%
Guest Skeptic: Dr. Stephen Meigher is the EM Chief Resident training with the Jacobi and Montefiore Emergency Medicine Residency Training Program. Guest Skeptic: Dr. Stephen Meigher is the EM Chief Resident training with the Jacobi and Montefiore Emergency Medicine Residency Training Program. The TOMAHAWK Investigators.
EMS arrived and found him in Ventricular Fibrillation (VF). Then assume there is ACS. Cardiac arrest #3: ST depression, Is it STEMI? This patient was witnessed by bystanders to collapse. They started CPR. He was defibrillated into VT. He then underwent dual sequential defibrillation into asystole. sodium bicarbonate.
While STEMI negative, the ECG is diagnostic of proximal LAD occlusion. Transient STEMI” are often managed like non-STEMI with delayed angiography, which is very risky. This case is an example of the steps we can all take in daily practice as the paradigm shifts from STEMI to OMI.
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]
He called EMS, who arrived on scene about two hours after the onset of pain to find him hypertensive at 220 systolic. The cardiologist recognized that there were EKG changes, but did not take the patient for emergent catheterization because the EKG was “not meeting criteria for STEMI”. The ST depressions in I and aVL have resolved.
He presented to EMS with extreme pallor, Levine sign, diaphoresis, bilateral arm pain, and an apprehensive sense of doom. It should be emphasized here that this is a presentation of high-pretest probability for Acute Coronary Syndrome (ACS). In the case of ACS, the ECG can rapidly change from this. ECG's are difficult.
He reported to EMS a medical history of GERD only. 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. However, in this context (i.e.
Pain improved to 1/10 after EMS administers 324 mg aspirin and the following EKG is obtained at triage. 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." looked at consecutive patients with PE, ACS, or neither. What do you think?
Written by Bobby Nicholson What do you think of this “STEMI”? With EMS, patient had a GCS of 3 and was saturating 60% on room air. He improved to 100% with the addition of non-rebreather, however remained altered and was intubated by EMS with ketamine and succinylcholine. The patient is unconscious and hypoxic. ng/mL and 0.10
All patients with NSTE-ACS ( NSTEMI or unstable angina) are treated similarly with respect to anti-ischemic and anti-thrombotic drugs. Guidelines recommend the use of validated risk models to estimate the risk of acute myocardial infarction , 30-days and 1-year mortality in patients with NSTE-ACS.
About 2 hours later the patient arrived at a PCI-capable center and repeat ECG was obtained: The transferring EMS crew noted “runs of VT” during transport. The receiving emergency physician consulted with interventional cardiology who stated there was no STEMI. Is there STEMI? I suspect the EMS crew misdiagnosed AIVR as VT.
He had multiple cardiovascular risk factors and the EM physician strongly suspected ACS. Over the next few hours, four other general cardiologists "signed off on the initial ECG without recognizing STEMI." Learning Points: STEMI criteria misses 25-40% of OMI, like this case for example. mm of the "required" 1.0
EMS obtained the following vital signs: pulse 50, respiratory rate 16, blood pressure 96/49. It appears EMS obtained two EKGs, but unfortunately these were not saved in the medical record. The EMS crew was only BLS certified, so EKG interpretation is not within their scope of practice.
Is this inferor STEMI? Atrial Flutter with Inferior STEMI? Inferolateral ST elevation, vomiting, and elevated troponin The treating team did not identify the flutter waves and they became worried about possible "STEMI" (despite the unusual clinical scenario). The EM provider asked if the cardiologist thought it was a "STEMI."
Figure 1-1 My colleague, a faithful student of ECG interpretation, handed me the tracing and said that it warranted STEMI activation because of apparent terminal QRS distortion (TQRSD) in V2. Anecdotally, had there been symptoms unequivocally consistent with ACS then one could justifiably make the case for a potential D1 occlusion.
The ECG was read as "No STEMI" and the patient was treated like an average chest pain patient (despite the fact that a chest pain patient with active pain and active subendocardial ischemia is very high risk). In our opinion it should not be given in ACS unless you are committed to the cath lab. He was diagnosed as NSTEMI.
There is a very small amount of STE in some of the anterior, lateral, and inferior leads which do NOT meet STEMI criteria. One must always be careful when looking for "baseline" ECGs, because the prior ECG on file may have been during another ACS event, as this one clearly was. This ECG is highly suspicious for LAD OMI.
This is technically a STEMI, with 1.5 However, I think many practitioners might not see this as a clear STEMI, and would instead call this "borderline." They collected several repeat ECGs at the outside hospital before transport: None of these three ECGs meet STEMI criteria. This ECG was recorded on arrival: What do you think?
STEMI was activated and the patient went to Cath on arrival. Such aggressive investigation was particularly warranted in this case because of symptoms compatible with ACS, as well as an equally frightening revelation of family history. Conjecture aside, I believe the lesson here, ultimately, is serial ECG’s.
A 60-something man presented by EMS with 5 hours of fairly typical sounding substernal chest pain. Here is the EMS ECG: Obviously massive diffuse subendocardial ischemia, with profound STD and STE in aVR Of course this pattern is most often seen from etoliogies other than ACS. Is this OMI?
Step 1 to missing posterior MI is relying on the STEMI criteria. A prospective validation of STEMI criteria based on the first ED ECG found it was only 21% sensitive for Occlusion MI, and disproportionately missed inferoposterior OMI.[1] But it is still STEMI negative. A 15 lead ECG was done (below). In a study last year, 14.4%
This case was provided by Spencer Schwartz, an outstanding paramedic at Hennepin EMS who is on Hennepin EMS's specialized "P3" team, a team that receives extra training in advanced procedures such as RSI, thoracostomy, vasopressors, and prehospital ultrasound. From Gue at al.
Today’s pain lasted around 20 mins, but was severe enough that the patient called EMS. Pain largely resolved prior to EMS arrival but completely subsided after prehospital NTG and aspirin. Practice putting the probe on the chest of someone with an obvious STEMI(+) OMI in order to look for regional wall motion abnormalities.
Sent by Anonymous, written by Pendell Meyers A man in his 60s with history of CAD and 2 prior stents presented to the ED complaining of acute heavy substernal chest pain that began while eating breakfast about an hour ago, and had been persistent since then, despite EMS administering aspirin and nitroglycerin.
It may be difficult to read STEMI in the setting of RBBB. There is, however, a long QT also, with abnormal T-waves, but this is not STEMI. This ECG was recorded prehospital, and the computer read STEMI, so the medics activated the cath lab: What do you think? The ECG is consistent with high lateral STEMI. Called 911.
It was edited by Smith CASE : A 52-year-old male with a past medical history of hypertension and COPD summoned EMS with complaints of chest pain, weakness and nausea. Clinical Course The paramedic activated a “Code STEMI” alert and transported the patient nearly 50 miles to the closest tertiary medical center. What do you see?
If this is ACS with Aslanger's pattern , the ST depression vector of subendocardial ischemia (due to simultaneous 3 vessel or left main ACS) is directed toward lead II (inferior and lateral). Thus, this apparently is Aslanger's Pattern (inferior OMI with single lead STE in lead III, with simultaneous subendocardial ischemia).
He had received aspirin and nitroglycerin by EMS, with some improvement. Corroborating this is the subtle ST depression in V2-V3 which is inappropriate for the normal QRS complex, and in the context of ACS, we have shown this is quite specific for posterior OMI. His vitals were within normal limits.
Jesse McLaren on when to consider Spontaneous Coronary Artery Dissection (SCAD), which patients are at risk for reocclusion, and the challenges of diagnosing SCAD in patients who have nonischemic ECGs despite silent occlusion, occlusions perfused by collaterals, or from non-occlusive MI on this ECG Cases.
This post was written by Tarissa Lai, one of our outstanding EM residents at Hennepin County Medical Center, with comments by Steve Smith and Dan Lee. female with HTN, HLD, diabetes, ESRD on dialysis is brought in by EMS with sudden onset, left -sided chest pain for the past four hours. Case A 30 something y.o.
The patient contacted EMS after a few hours of chest pain that started 5:30 AM. ECG #2 QoH interpretation of ECG #2 Generally when patients are accepted for emergent evaluation in the cath lab, the EMS service keeps the patient connected to the twelve lead ECG during transport. He is otherwise healthy.
You must understand this and the dynamic nature of ACS to provide excellent care for such patients. Failure to do so may result in overlooking subtle ST-T wave changes in a patient "in passage" from a frank STEMI toward reperfusion changes. Serial ECGs are important to perform and incredibly helpful at all stages of expertise.
PMID: 30060961 Koller AC, et al. As above, we take the PCAC score into account when we order our interventions and may prioritize Neuroresuscitation in a PCAC 4 over a cath without a hard indication (STEMI). Epub 2016 Jun 28. PMID: 27368428 Elmer J, et al. Ann Emerg Med. Epub 2018 Jul 4. Resuscitation.
Written by Jesse McLaren A 75 year old with a history of CABG called EMS after 24 hours of chest pain. STEMI negative : the EMS automated interpretation read, “STEMI negative. Even if the patient had presented acutely with STEMI criteria, the ST elevation resolved on arrival though the pain continued.
He has a history of coronary artery disease and a STEMI two years prior that was treated with primary PCI. He contacted EMS due to acute onset chest pain and feeling unwell and fatigued. These are obvious OMI findings that do not meet STEMI criteria. He was given ASA and sublingual NTG and taken to the ED.
Written by Pendell Meyers, sent by anonymous, with additions by Smith A man in his 40s had acute chest pain and called EMS. EMS arrived and recorded this ECG: What do you think? Here is the PMcardio Queen of Hearts interpretation of the ECG: STEMI equivalent detected. Inferior and posterior OMI without STEMI criteria.
The Case An 88-year-old woman with a history of dementia, major depressive disorder, and hyperlipidemia presented to the ED via EMS after a near syncopal episode. EKG is concerning for acute STEMI with STE in lead I and aVL with reciprocal changes. EKG is concerning for acute STEMI with STE in lead I and aVL with reciprocal changes.
Background: ST-segment elevation myocardial infarction (STEMI) is a critical condition requiring rapid diagnosis and intervention. While ECGs play a central role in detecting STEMI, misinterpretations often occur, leading to unnecessary catheterization or missed diagnoses. 5991 ECGs with Normal annotation and 79 STEMI ECGs.
EMS arrived and recorded this ECG: What do you think? The is very small STE in III and aVF which do not meet STEMI criteria, hyperacute T waves, reciprocal TWI in aVL, and maximal STD in V2-V3 showing posterior OMI. The cath lab was activated despite lack of STEMI criteria, around 2 am in the morning. Very frustrating.
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