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By Magnus Nossen This ECG is from a young man with no risk factors for CAD, he presented with chestpain. The patient is a young adult male with chestpain. The chestpain was described as pressure like and radiation to both arms and the jaw. How would you assess this ECG? What is your next step?
Sent by Magnus Nossen MD, written by Pendell Meyers A man in his 50s, previously healthy, developed acute chestpain. The primary care physician there evaluated this patient and deemed the chestpain to be due to gastrointestinal causes. Clinical Cardiology 2019. No troponins were measured!
Written by Magnus Nossen with Edits by Grauer and Smith The ECGs in today’s case are from 3 different patients all presenting with new-onset CP ( ChestPain ). In any case, the ECG is diagnostic of severe ischemia and probably OMI. All ECGs were recorded by EMS, and transferred to a PCI capable center for evaluation.
Written by Jesse McLaren Four patients presented with chestpain. Other signs of OMI that complement the ECG include new regional wall motion abnormalities and refractory ischemia References 1. 2019 ; 54 : 79 - 81. Hughes KE , Lewis SM , Katz L , Jones J. Acad Emerg Med. 2017 ; 24 ( 1 ): 120 - 124 2. Am J Emerg Med.
[link] A 30 year-old woman was brought to the ED with chestpain. She had given birth a week ago, and she had similar chestpain during her labor. She attributed the chestpain to anxiety and stress, saying "I'm just an anxious person." This strongly suggests reperfusing RCA ischemia.
The patient presented with chestpain. 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. chestpain for the ischemia and potential syncope for brugada.
This is a previously healthy male teenager who was awoken by chestpain. The pain is described as located in the midsternal area, radiating to the right arm, described as 8-9/10 and worse with deep inspirations. In the evening, he became diaphoretic and complained of 9/10 continuous chestpain.
Written by Jesse McLaren, with comments from Smith and Grauer A 60 year old presented with three weeks of intermittent non-exertional chestpain without associated symptoms. A prospective validation of the HEART score for chestpain patients at the emergency department. JAMA Intern Med 2019 9. Int J Cardiol 2013 2.
He then went on to say: "40-something with chestpain for one hour. Burning pain subxiphoid and into throat." It does not usually represent subendocardial ischemia, but rather it is usually reciprocal ST depression, reciprocal to inferior ST elevation. (But Had episode of nausea and dizziness when it started.
Case written and submitted by Ryan Barnicle MD, with edits by Pendell Meyers While vacationing on one of the islands off the northeast coast, a healthy 70ish year old male presented to the island health center for an evaluation of chestpain. The chestpain started about one hour prior to arrival while bike riding.
A 50-something male who is healthy and active with no previous medical history presented with 5 hours of continuous worrisome chestpain. Chestpain with New LBBB: It helps to actually measure the ST/S ratio A Fascinating Demonstration of ST/S Ratio in LBBB and Resolving LAD Ischemia The cath lab was activated.
2 days later This is a typical LVH pattern, without ischemia Patient underwent 4 vessel CABG. Upon questioning patient, he denies having any chestpain or chest tightness of any sort. Pericarditis would be even more unlikely in someone without chestpain. Chestpain is squeezing or tight in nature.
He woke up alert and with chestpain which he also had experienced intermittently over the previous few days. The first task when assessing a wide complex QRS for ischemia is to identify the end of the QRS. His wife contacted the ambulance service after the patient experienced an episode of loss of consciousness.
He did not have chestpain. A prior ECG was available for comparison: Normal One might be tempted to interpret the ST depression as ischemia, but as Smith says, "when the QT is impossibly long, think of hypokalemia and a U-wave rather than T-wave." Chestpain in high risk patient. Is it STEMI?
As a result, the ST elevation ( with especially tall, peaked T wave in lead V2) — is not indication of acute ischemia. Today's patient is a middle-aged woman who presented with low back pain, shortness of breath and marked hypertension — but no chestpain.
On the day of presentation she complained of typical chestpain, and stated it feels like prior MI. ECG#1 Assessing ischemia on an ECG with wide QRS complexes (AIVR, ventricular pacing, BBB, etc) can be challenging. Many health care providers will simply not attempt to assess ischemia in the presence of a wide QRS.
Subendocardial Ischemia from another Cause ( ie, sustained tachyarrhythmia; cardiac arrest; shock or profound hypotension; GI bleeding; anemia; "sick patient" , etc. ). To EMPHASIZE: This pattern of diffuse Subendocardial Ischemia does not suggest acute coronary occlusion ( ie, it is not the pattern of an acute MI ).
My written interpretation on a tracing such as this one would read, "Marked LVH and 'strain' and/or ischemia — with need for clinical correlation." BOTTOM Line: Today's patient presented with a 2-3 day history of chestpain and the ECG shown in Figure-1.
When I was shown this ECG, I said it looks like such widespread ischemia that is might be a left main occlusion, or LM ischemia plus circumflex occlusion (high lateral and posterior OMI). Here are some cases of RBBB with LAFB: What is the Diagnosis in this 70-something with ChestPain? There is STE in aVR.
Written by Willy Frick A 50 year old man with no medical history presented with acute onset substernal chestpain. In this patient's case, the RV ischemia manifested as dramatic anterior hyperacute T waves. This degree of STE is a bit atypical for LAD ischemia. His ECG is shown below.
The ECG in Figure-1 was obtained from a 90-year old woman — who presented with a 2-to-3 day history of chestpain, that became worse on the day of admission. The terminology favored to describe these ECG findings is diffuse subendocardial ischemia ( See ECG Blog #271 — for more on diffuse subendocardial ischemia ).
Context: a man in his 40s presented to the emergency department with 1 day of sudden onset chestpain. That said — I did not interpret these differences as the result of acute ischemia. I sent this to our group without information and Dr. Smith responded: "Not OMI. Pericarditis maybe."
A 60-something man presented by EMS with 5 hours of fairly typical sounding substernal chestpain. 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.
The patient in today’s case is a previously healthy 40-something male who contacted EMS due to acute onset crushing chestpain. The pain was 10/10 in intensity radiating bilaterally to the shoulders and also to the left arm and neck. There is no definite evidence of acute ischemia. (ie, The below ECG was recorded.
He arrived to the ED by helicopter at 1507, about three hours after the start of his chestpain while chopping wood around noon. He arrived to the ED by ambulance at 1529, only a half hour after the start of his chestpain around 1500 while eating. Still, such dramatic changes cannot be overlooked.
A middle aged man had off and on chestpain for 2 weeks, then 2 hours of more severe and constant pain. Contrary to what Ken stated, the ST vector remains mostly posterior __ What about subendocardial ischemia? Similarly, STD in aVL is usually reciprocal to inferior ST elevation, not "lateral ischemia."
But, in a patient who presents to the ED for new chestpain — seeing these subtle findings that are localized to leads V2- thru -V4 should at the least make you consider acute posterior OMI ( O cclusion-based MI ) — until you prove otherwise. To EMPHASIZE: These are subtle findings. What do YOU think?
A middle-aged woman with history of hypertension presented to another hospital approximately 2 hours after onset of chestpain and shortness of breath. I believe this is by far the most common outcome for this patient around the world in 2019. This ECG was recorded on arrival: What do you think? mm STE in V1 and 1.5-2.0
The best course is to wait until the anatomy is defined by angio, then if proceeding to PCI, add Cangrelor (an IV P2Y12 inhibitor) I sent the ECG and clinical information of a 90-year old with chestpain to Dr. McLaren. His response: “subendocardial ischemia. Am J Med 2019, 132(5):622-630. Anything more on history?
The only time you see this without ischemia is when there is an abnormal QRS, such as LVH, LBBB, LV aneurysm (old MI with persistent STE) or WPW." Here is the patient's troponin I profile: These were interpreted as due to demand ischemia, or type II MI. ng/mL is seldom a result of demand ischemia (type 2 MI). First was 2.9
This fantastic case and post was written by Jesse McLaren (@ECGcases), edited by Smith Case You’re shown an ECG from a patient in the waiting room with chestpain. It was a 60yo with a history of stents to the circumflex and right coronary arteries, who presented with 9 hours of fluctuating central chestpain.
or basilar ischemia. Not a STEMI: Reasons I did not think ECG #1 represented an acute STEMI — included the following: There was no history of chestpain. EKG on arrival to the ED is shown below: What do you think? On my initial interpretation, the patient has normal sinus rhythm with a narrow QRS complex, and LVH.
She did not report any chestpain or pressure. She was brought to the Emergency Department and this ECG was recorded while she was still feeling nauseous but denied chestpain, shortness of breath, or other symptoms: What do you think? The morphology of STE is not diagnostic of being due to acute transmural ischemia.
The patient was a 70-something yo previously healthy male on no medications who presented to the ED with epigastric pain, onset over a few hours. He denied chestpain of any sort and his vitals were all normal. They cannot be assumed due to LV strain ( and they cannot be assumed to represent ischemia ).
This patient's ischemia was so brief that it did not cause any myocardial stunning. The patient is a 40-something year old man with new chestpain. In a patient with new chestpain — these T wave changes for beats labeled “ B ” in leads V1 , V2 and V3 constitute h yperacute T waves ! The QTc is normal.
A 40-something woman with diabetes and peripheral vascular disease who frequently needs the ED for chronic pain called 911 for sudden severe chestpain. Does this mean that the ST depression in V3 represents "anterior" subendocardial ischemia, and not posterior OMI? non-occlusive ischemia) 2.
Share ChestPain Symptoms There is no role for CT Calcium Scoring in the setting of someone with chestpain symptoms suspected to be from a narrowed coronary artery. Regardless, if you present with chestpain and get a stress test instead of a CTCA, you are arguably getting an inferior test. I would say yes.
Part of the ST depression with deep T wave inversion in the lateral chest leads clearly reflects LV "strain" from the marked LVH — but despite the very large QRS amplitudes, this ST-T wave appearance looks disproportionate, suggesting at least a component of ischemia.
He was asked multiple times about chestpain or dyspnea, but repeatedly denied any such symptoms. Patient denied chestpain on initial review of symptoms. Was now endorsing chestpain which began 30 minutes ago. Upon further questioning, he states that he has had intermittent chestpain since yesterday.
Inferior ST Depression does NOT mean there is inferior subendocardial ischemia; it is generally reciprocal to high lateral (aVL) subepicardial ischemia (OMI/STEMI) == MY Comment by K EN G RAUER, MD ( 2/10/2023 ): == There are certain patterns in ECG interpretation that experienced providers are able to immediately recognize.
There is broad subendocardial ischemia as demonstrated by STE aVR with concomitant STD that almost appears appropriately maximal in Leads II and V5. There is LBBB-like morphology with persistent patterns of subendocardial ischemia. This is the initial ECG: The QRS is widened with a regular cadence, and there are no discernable P waves.
The patient contacted EMS after a few hours of chestpain that started 5:30 AM. The pain was described as 6/10 radiating to the right shoulder. The chestpain was described as both sharp and pressure like. He is otherwise healthy. Vital signs were within normal limits, and the patient was not ill appearing.
If a patient presents with chestpain and a normal heart rate, or with shockable cardiac arrest, then ischemic appearing ST elevation is STEMI until proven otherwise. This, in turn, could produce platelet aggregation and vasospasm and result in an acute coronary syndrome." Clinical Context is everything !
Weren't you taught that "new tall T wave in V1" is concerning for ischemia, and so this is the opposite? Meyers, are the only leads thus far for which data documents the diagnostic benefit of this finding ( For brief review + illustration of T-QRS-D — SEE My Comment at the bottom of the November 14, 2019 post).
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