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We discover that for STEMI/OMI vs subendocardial ischemia, we should look for STEMI(-)OMI, subacute OMI, and OMI in the presence of LBBB and RBBB, and consider the differential for diffuse ST depression with reciprocal ST elevation in aVR.
A 63 year old man with a history of hypertension, hyperlipidemia, prediabetes, and a family history of CAD developed chest pain, shortness of breath, and diaphoresis after consuming a large meal at noon. He called EMS, who arrived on scene about two hours after the onset of pain to find him hypertensive at 220 systolic. Smith SW.
He had some cardiac risk factors including hypertension, on meds, but no previous coronary disease. He had an immediate ED ECG: There is artifact, but the findings appear to be largely gone now The diagnosis is acute MI, but not STEMI. There is about 1 mm of STE in aVR I con sidered but rejected subendocardial ischemia.
He interprets here: "This EKG is diagnostic of right bundle branch block and transmural ischemia of the anterior wall, most likely from an occlusion of the proximal LAD. It was recorded at 0530: What do you think? The young ED tech immediately suspected LAD OMI. There is a hyperacute distribution of T waves from V1 to V4.
Written by Pendell Meyers, few edits by Smith A man in his 60s with history of stroke and hypertension but no known heart disease presented with chest pain that started on the morning of presentation at around 8am. So it is very unclear to me whether or not "posterior STEMI" is actually a recognized entity under our current guidelines.
Written by Willy Frick A man in his 50s with history of hypertension, hyperlipidemia, and a 30 pack-year smoking history presented to the ER with 1 hour of acute onset, severe chest pain and diaphoresis. The fact that R waves 2 through 6 are junctional does make ischemia more difficult to interpret -- but not impossible. ng/mL (ref. <
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?
A 50-something man with history only of alcohol abuse and hypertension (not on meds) presented with sudden left chest pain, sharp, radiating down left arm, cramping, that waxes and wanes but never goes completely away. If this STD were due to LVH or to subendocardial ischemia, rather than posterior OMI, it would be maximal in V5 and V6.
Her vitals signs were remarkable for marked hypertension. 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." The criteria of Armstrong et al. References 1.
Sent by anonymous, edited by Pendell Meyers A man in his 50s with history only of hypertension presented with acute chest pain that started 45 minutes prior to presentation while doing yard work. Post Cath ECG: Obviously completing MI with LVA morphology, and STE that meets STEMI criteria (but pt is still diagnosed as "NSTEMI").
Case submitted and written by Mazen El-Baba MD, with edits from Jesse McLaren and edits/comments by Smith and Grauer A 90-year old with a past medical history of atrial fibrillation, type-2 diabetes, hypertension, dyslipidemia, presented with acute onset chest/epigastric pain, nausea, and vomiting. His response: “subendocardial ischemia.
It has been estimated that in the aggregate, they occur at a rate of about 3 per 1000 patients with acute MI, and most of these events occur in patients with STEMI. A mong patients with STEMI, ventricular septal rupture is the most common and free wall rupture is the least common.
A woman in her 40's who was healthy, except for hypertension, was at work when she suddenly complained of neck and shoulder pain and then collapsed. STE limited to aVR is due to diffuse subendocardial ischemia, but what of STE in both aVR and V1? Was this: 1) ACS with ischemia and spontaneous reperfusion? see below).
This was a male in his 50's with a history of hypertension and possible diabetes mellitus who presented to the emergency department with a history of squeezing chest pain, lasting 5 minutes at a time, with several episodes over the past couple of months. New ST elevation diagnostic of STEMI [equation value = 25.3 Gottlieb SO, et al.
A man in his 70s with past medical history of hypertension, dyslipidemia, CAD s/p left circumflex stent 2 years prior presented to the ED with worsening intermittent exertional chest pain relieved by rest. The baseline ECG is basically normal with no ischemia. In my opinion, I think it looks more like subendocardial ischemia.
It is due to transmural ischemia not only of the anterior wall and apex, but due to transmural ischemia of the septum, usually due to occlusion proximal to the first septal perforator. As always, LAD OMI need not meet STEMI criteria and usually does NOT! Is this Acute Ischemia? The voltage is high but not huge.
She is somewhat hypertensive, but her vital signs are otherwise normal. These elevations meet STEMI criteria ( ≥ 1mm in 2 contiguous leads). While this may be change that is reciprocal to an Acute/Subacute Inferior STEMI, the problem is that LV aneurysm may also manifest with this reciprocal change. This case is tough.
The computer calls it a STEMI. Never chest pain but had to treat as hypertensive emergency. In fact, severe hypertension by itself can lead to greatly increased oxygen demand and type 2 acute MI, sometimes with ST Elevation. See this case of Type 2 STEMI due to severe hypertension. Here are more Type II STEMI.
His medical history includes hypertension, a decade-long battle with diabetes, ischemic heart disease, a coronary bypass graft surgery ten years ago, a diagnosis of congestive heart failure for the last five years, and a prior ICD implantation five years ago. The patient rapidly regained consciousness, reporting no residual pain.
Jesse McLaren (@ECGcases), of Emergency Medicine Cases Reviewed by Pendell Meyers and Steve Smith An 85yo with a history of hypertension developed chest pain and collapsed, and had bystander CPR. The patient was brought to the ED as a possible Code STEMI and was seen directly by cardiology. Learning points 1.
There is normal R-wave progression in the precordial leads with no evidence of ischemia. Any cause of pulmonary hypertension. Troponin T peaked at 2074 ng/L (very high, typical of OMI/STEMI). Here the image quality is enhanced using the PM Cardio app. What do you think? The presenting ECG shows SR with narrow QRS complexes.
There is ventricular hypertrophy in the absence of abnormal loading conditions, such as aortic stenosis, or hypertension, for example – of which the most common variant is Asymmetric Septal Hypertrophy. There is LBBB-like morphology with persistent patterns of subendocardial ischemia.
This meets "STEMI criteria" However, there is very high voltage, with a very deep S-wave in V2 and tall R-wave in V4. The morphology is not right for STEMI. My interpretation: LVH with secondary ST-T abnormalities, exaggerated by stress, not a STEMI. This is very good evidence that the ST elevation is not due to STEMI.
He had a history of hypertension but stopped taking his medication several years ago. Wellens' syndrome represents the aftermath of an unrecorded occlusion (STEMI) with spontaneous reperfusion. In such cases, if there is no infarction (necrosis), when the ischemia resolves, the T-wave may normalize (in contrast to Pseudo-normalize).
Although as a general rule, there should be no ST elevation in RBBB in the absence of ischemia, there sometimes is ST elevation that looks like this. There is also much STE in V3-V6, especially V4-V6, that must be considered to be STEMI. The challenge is magnified when trying to assess BBB tracings for acute ischemia.
The Queen of Hearts correctly says: Smith : Why is this ECG which manifests so much ST Elevation NOT a STEMI (even if it were a 60 year old with chest pain)? He was mildly tachycardic (105-110 bpm) and hypertensive (157/92 mm Hg) on arrival. Physician interpretation: "No STEMI." Physician: "No STEMI."
A 56 year old male with a history of diabetes, dyslipidemia, hypertension, and coronary artery disease presented to the emergency department with sudden onset weakness, fatigue, lethargy, and confusion. At 2111, the troponin I peaked at 12.252 ng/mL (this is in the range of STEMI patients, quite high).
The patient was in his 50s with history of hypertension, diabetes, seizure disorder, and smoking, but no known coronary artery disease. He wrote in his note that "The EKG showed early repolarization in I, V2-V3 but no clear STEMI pattern." See far below for data on 24 troponin T in STEMI and NSTEMI, and correlation with infarct size.
Sent by Drew Williams, written by Pendell Meyers A man in his 50s with history of hypertension was standing at the bus stop when he developed sudden onset severe pressure-like chest pain radiating to his neck and right arm, associated with dyspnea, diaphoresis, and presyncope. Is this Acute Ischemia? When is it anterior STEMI?
Here is a repeat ECG 45 minutes later with persistent chest pain: Obviously progressing into a clear STEMI. Meets formal STEMI criteria in V2-V3. The ECG was interpreted as non-ischemic. The patient was closely monitored. Also notice clearly hyperacute T waves in V2-V4, as well as worsening STD in V5-6 and II, III, aVF.
This patient, who is a mid 60s female with a history of hypertension, hyperlipidemia and GERD, called 911 because of chest pain. A mid 60s woman with history of hypertension, hyperlipidemia, and GERD called 911 for chest pain. This has resulted in an under-representation of STEMI MINOCA patients in the literature.
Diffuse ST depression with ST elevation in aVR: Is this pattern specific for global ischemia due to left main coronary artery disease? Ischemia b. ST depression: is it ischemia? Does this patient have hypertension and/or heart failure that has worsened? It was a baseline finding in 62% of patients, usually due to LVH.
Written by Pendell Meyers A woman in her 70s with diabetes, hypertension, and hyperlipidemia suddenly developed nausea, diaphoresis, and brief syncope while eating at a restaurant. The morphology of STE is not diagnostic of being due to acute transmural ischemia. This one likely does meet STEMI criteria in II, III, and aVF.
edits by Meyers A woman in her 60s with a history of chronic atrial fibrillation on Eliquis, ESRD on hemodialysis, type-II diabetes mellitus, prior CVA, hypertension, and hyperlipidemia presented to the emergency department with multiple complaints after missing dialysis. Is this inferor STEMI? Atrial Flutter with Inferior STEMI?
This is by Magnus Nossen, from Norway The patient is a 70 something male with a hx of hypertension and tobacco use disorder. In other words, the inferior ST segments in the first ECG show more straightening which is more concerning for ischemia. He is otherwise healthy. The pain was described as 6/10 radiating to the right shoulder.
But lead V2 has a worrisome amount of ST elevation, and in a chest pain patient, I would be worried about STEMI. But in a patient without any such symptoms — marked LVH in a patient with severe longstanding hypertension may sometimes produce very similar ST-T wave changes as are seen in Figure-1. The Ratios of STE to S-wave: V1: 2.5/16
They recorded a prehospital ECG and diagnosed STEMI and activated the cath lab prehospital. This ST-T wave appearance in the lateral chest leads of ECG #2 is consistent with L V “ S train” vs ischemia. When medics arrived, he denied any chest pain, shortness of breath, or palpitations prior to the syncopal episode.
The patient stated he had a long history of well-controlled hypertension for which he was compliant with his ACE-inhibitor. These findings are concerning for inferior wall ischemia with possible posterior wall involvement. He was also treated for erectile dysfunction but had not taken any medications recently.
He was hypertensive and tachycardic, with mildly increased work of breathing. The axiom of "type 1 (ACS, plaque rupture) STEMIs are not tachycardic unless they are in cardiogenic shock" is not applicable outside of sinus rhythm. Is that an obvious STEMI underneath that rhythm? Here is his initial ECG: What do you think?
Here is his ED ECG: There is obvious infero-posterior STEMI. What are you worried about in addition to his STEMI? Comments: STEMI with hypokalemia, especially with a long QT, puts the patient at very high risk of Torsades or Ventricular fibrillation (see many references, with abstracts, below). There is atrial fibrillation.
Written by Pendell Meyers A man in his late 30s with history of hypertension, tobacco use, and obesity presented to the Emergency Department for acute chest pain which started approximately 3 hours prior to arrival, in the setting of a very stressful situation. Vitals were within normal limits except some hypertension. Which is true.
Written by Kaley El-Arab MD, edits by Pendell Meyers and Stephen Smith A 61-year-old male with hypertension and hyperlipidemia presented to the emergency department for chest tightness radiating to the back of his neck that has been intermittent for the past day or two. This ECG was read as “No STEMI” with no prior available for comparison.
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. Then there is the significant ST elevation we see in lead V1.
There is appreciable STE aVR with near-global STD that appropriately maximizes in Leads II and V5, and thus suggesting a circumstance of generic, diffusely populated, circumferential subendocardial ischemia versus occlusive coronary thrombus. [1] The patient was found to be hypertensive and treated accordingly.
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