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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.
A 56 year old male with PMHx significant for hypertension had chest pain for several hours, then presented to the ED in the middle of the night. No ischemia. An inferior wall motion abnormality does NOT say that there is active ischemia because previous ischemia will result in persistent wall motion abnormality (stunning).
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. There was a 100% proximal LAD occlusion that was opened and stented. It was recorded at 0530: What do you think? The young ED tech immediately suspected LAD OMI.
He was hypertensive and tachycardic, with mildly increased work of breathing. In some cases the ischemia can be seen "through" the flutter waves, whereas in other cases the arrhythmia must be terminated before the ischemia can be clearly distinguished. Here is his initial ECG: What do you think? How many problems does he have?
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.
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? It was stented.
Common comorbidities included hypertension (62.5%), smoking (56.3%), and hyperlipidemia (46.9%). Of the 32 patients, 9(28.1%) had dissection with diagnostic angiograms, 6(18.8%) endovascular thrombectomy, 15(46.9%) aneurysm treatment, and 2(6.3%) angioplasty with or without stenting. Only 4(12.5%) were treated with hyperacute stenting.
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.
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.
Case submitted and written by Dr. 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. So there is now high pre-test probability + refractory ischemia + Modified Sgarbossa + dynamic ECG changes.
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. It was stented. Comment: most T-wave inversion is nonspecific, but not these ones!
Written by Willy Frick A man in his 50s with a history of hypertension, dyslipidemia, type 2 diabetes mellitus, and prior inferior OMI status post DES to his proximal RCA 3 years prior presented to the emergency department at around 3 AM complaining of chest pain onset around 9 PM the evening prior. Peak troponin was 12 ng/mL.
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. Two stents were placed with resultant TIMI 3 flow.
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. The patient’s angiogram should have been expedited, but the EKG change was not recognized as recurrence of transmural ischemia.
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.
Normally, concavity in ST segments suggests absence of anterior ischemia (though concavity by itself is not reassuring - see this study ). It was thought to be an in stent restenosis and thrombosis from a DES placed in the same region 6 months prior. In there ECG evidence of possible ongoing ischemia? (ie, Herzog et al.
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. The culprit lesion was opened and stented. He is otherwise healthy.
Written by Pendell Meyers, edits by Steve Smith A man in his 60s with history of hypertension and MI 10 years ago, with PCI, presented to an outside hospital complaining of chest pain that started while mowing the lawn. The LAD lesion was acute and required 3 stents to restore flow. Here is his ECG on arrival: What do you think?
She is somewhat hypertensive, but her vital signs are otherwise normal. Ischemic Hyperacute T waves (Tall, round, symmetric, vs the “pointy” peaked-T’s of HyperK), are often a clue to ischemia. She received PCI with 2 drug-eluting stents in overlying fashion. This was written by Sam Ghali ( @ EM_RESUS ), with a few edits by me.
Edits by Meyers and Smith A man in his 70s with PMH of hypertension, hyperlipidemia, type 2 diabetes, CVA, dual-chamber Medtronic pacemaker, presented to the ED for evaluation of acute chest pain. So the patient was taken for emergent cath, showing: Culprit artery: LAD (100% stenosis, TIMI 0) requiring thrombectomy and stent.
Her vitals signs were remarkable for marked hypertension. All these factors, again, support an ECG diagnosis of LVH The patient was nonetheless taken for emergency angiography, and a 99% mid-LAD lesion was found and stented. It is unclear if ischemia modifies T wave height or morphology in LVH. 3 Is the STE concave or convex?
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. Slow TIMI 2 initially with brisk flow status post percutaneous coronary intervention with 18mm drug-eluting stent.
Women also had more cardiovascular risk factors, including hypertension (66.6% The diagnosis typically requires classic clinical features, with no evidence of obstructive coronary disease, and typical findings of ischemia on functional studies. versus 63.2%; P <0.001), hyperlipidemia (68.9% versus 66.3%; P =0.004), older age (62.4±7.9
This was stented. If there is polymorphic VT with a long QT on the baseline ECG, then generally we call that Torsades, but Non-Torsades Polymorphic VT can result from ischemia alone. I have read articles that say that patients without ischemia are at low risk of complications from hypokalemia, But it is not entirely without risk.
Written by Willy Frick A 51 year old man with hypertension presented with three hours of acute onset, severe midsternal chest pain associated with two episodes of nausea and vomiting. The operator performed intravascular ultrasound and visualized acute plaque rupture with thrombus formation and placed a stent. ECG 1 What do you think?
Case A 76 year old man with chronic hypertension but no history of coronary disease or myocardial infarction presented to the ED with chest pain at 2343. His triage EKG is shown below: There is left bundle branch block, so the EKG must be evaluated for ischemia by Smith-modified Sgarbossa criteria. ST elevation has now developed in V6.
hypertension no other past history presented with 30 minutes of fluctuating non-radiating heaviness in chest, with diaphoresis and nausea. Here is the circumflex after stenting: Wide open The cardiologist called Dr. Lufkin back and said "Great call!!" This case was sent by an old residency friend, Kirk Lufkin. No cardiac past history.
Written by Magnus Nossen The ECG below was obtained from 50-something male with a history of hypertension and tobacco use. At cath there was a 100% proximal LAD occlusion, which was opened and stented. Transient ischemia may lead to "stunning". The ECG below ECG was recorded on the scene. How will you manage this patient?
Written by Willy Frick A man in his 60s with hypertension and prior stroke presented with three days of crushing chest pain. Unfortunately, although natively conducted beats are the best ones for evaluating ischemia, we only have a few! Moving on to ischemia , the ECG shows reperfused inferoposterolateral infarct.
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