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The ECG in Figure-1 — was obtained from a middle-aged woman with positional tachycardia and diaphoresis with change of position from suprine to sitting. Although CP ( C hest P ain ) was not a prominent symptom — ACS ( A cute C oronary S yndrome ) was suspected from the chest lead T wave inversion seen on this ECG. WHY — or Why Not?
Answer : Brainstem stroke specifically in the pons resulting in locked in syndrome. CT head without contrast 1 is performed and reveals the following: Question: What is the diagnosis?
Headpulse measurement can reliably identify large-vessel occlusion stroke in prehospital suspected stroke patients: Results from the EPISODE-PS-COVID study. The SGEM has covered LVO strokes several times (SGEM#137, SGEM#292, SGEM#333 and SGEM#349). Date: October 2, 2024 Reference: Paxton et al. Reference: Paxton et al.
Answer : Cerebellar Stroke Epidemiology: 1-4% of cerebrovascular accidents occur in the cerebellum. 2 In the United States, approximately 795,000 people suffer from strokes every year. 3 Cerebellar strokes are associated with high morbidity and mortality. CT head without contrast 1 reveals the following: What is the diagnosis?
CTA head and neck were obtained and showed no evidence of intracranial hemorrhage, large vessel occlusion stroke (what a helpful and apt name for an acute arterial occlusion paradigm, by the way.), EKG on arrival to the ED is shown below: What do you think? 2) There was no terminal QRS distortion on these ECGs. Any changes?
In the last post, we saw how important old ECGs are in assessing the current ECG in a patient without atypical presentation (in this previous case, the patient had no chest pain, and the apparent inferior OMI did not have reciprocal ST depression in lead aVL). Here is that last post: A 90-something with acute stroke.
Neurologist Hooman Kamel from the Weil Cornell Medical Center in NY had an idea about atrial fibrillation and stroke. Stroke came when these clots moved northward to the brain. One of the big issues with this theory was that studies had failed to show a strong relationship in time between the stroke and the irregular rhythm. (For
ECG Results: Repeat ECG 90min after tenecteplase indicated 70.3% ECG Results: Repeat ECG 90min after tenecteplase indicated 70.3% ECG Results: Repeat ECG 90min after tenecteplase indicated 70.3% The upper range of this time was 120 minutes from diagnostic ECG in the majority of patients.
Here is his triage ECG: What do you think? What is the most likely cause of the patient’s ECG findings, and what would be your first step in management? What does the ECG show? What does the ECG show? Figure-1: The initial ECG in this case — and a rapid method for estimating the QTc ( See text ). Is it STEMI?
A 90-something year old woman presented with an acute mild stroke. She had a routine ECG as part of her workup: What do you think? Peak trop 62 ng/L (would be very low for acute OMI) Next AM ECG: Still with very ischemic looking T-waves. Always look at old ECGs, even if you think the diagnosis is obvious.
. #1: Emergent Cath Lab Activations with “Normal” Computer ECG Interpretations Spoon Feed A significant minority of code STEMI patients have an initial normal computer ECG interpretation. Consequently, emergency physicians must remain vigilant to identify signs of OMI regardless of the initial computer ECG interpretation.
WHY IT MATTERS Classic heat stroke is a potentially deadly diagnosis that effects some of the most vulnerable of our populations. There are some key differences between exertional and classic heat stroke management and this case gives the opportunity to practice and discuss these skills.
Her heart rate was very fast, so we obtained an ECG immediately: ECG: What do you think? But the duration of symptoms was prolonged and so to avoid the risk of stroke, AV nodal blockade (rate control) was preferred. We want to avoid a stroke. WHY Did We Think Today's ECG was Supraventricular?
She is admitted with suspected stroke. Case 1: Excess An elderly woman is admitted to a community hospital with a minor stroke. The plan was that she would get a two-week, continuous EKG monitor placed and have a sleep study at this hospital. Sensible Medicine is a reader-supported publication. I love my job.
An ECG will also help with anaesthetic planning Bloods: CRP, U&E, FBC, LFTs, INR (if on warfarin), VBG (for lactate, pH and glucose), amylase Group and save: not all surgical procedures need group and saves- these are expensive and in many cases, unnecessary- check first!
His prehospital ECG was diagnostic of inferior posterior OMI. Here is his ED ECG: There is bradycardia with a junctional escape. We recorded an ECG in which V1-V3 were put in the position of V4R-V6R, and V4-6 were placed in V7-9 to (academically) confirm posterior OMI. The patient was in clinical shock with a lactate of 8.
Prehospital transdermal glyceryl trinitrate in patients with ultra-acute presumed stroke (RIGHT-2): an ambulance-based, randomized, sham-controlled, blinded, phase 3 trial. His 12-lead ECG shows a normal sinus rhythm without ST abnormality or ectopy. This episode will not debate the use of tPA for acute ischemic stroke.
For an older patient with stroke risk factors and 3 hours of AF on a cardiac device, pre-2023 thinking would have us leaning toward anticoagulation. Edoxaban reduced the primary endpoint of stroke, systemic embolism, and cardiovascular death by 19% (HR, 0.81; 95% CI, 0.60-1.08; The doctor would do an ECG and that would diagnose AF.
The ECG below was recorded by EMS. ECG #1 Interpretation: ECG #1 shows sinus rhythm at a heart rate of 77 bpm. At first glance, the ECG does not look too abnormal. In my experience, the pathologic finding in the above ECG is the easiest one to overlook — especially if you are in a rush and do not do a systematic review.
Here is the initial ED ECG. Other thought this was due to hyperkalemia, but the ECG does not have the appearance of hyperkalemia but does have the appearance of severe cardiomyopathy -- LBBB with very wide QRS) 3. Another ECG was recorded 12 minutes later: Paced rhythm, probable Pacemaker-Mediated Tachycardia ?
Here is her triage ECG: What do you think? And so was an appropriate anti-coagulant, since atrial flutter, like fibrillation, can result in thromboembolism and stroke. For clarity and ease of comparison, I've put together in Figure-1 — the 3 serial ECGs in today's case. Atrial flutter with 2:1 conduction.
Some background: In patients with certain risk factors, AF increases the risk of having a stroke. The increase in risk parallels the presence of risk factors, such as age, high blood pressure, diabetes, coronary disease, and previous stroke. Net benefit means stroke reduction > bleeding increase. We call this clinical AF.
The ECG below was recorded. The ECG was interpreted as showing atrial flutter with 2:1 conduction. Answer : The ECG above shows a regular wide complex tachycardia. Said differently, the ECG shows a rather slow ventricular tachycardia with a 2:1 VA conduction. How do you interpret the below ECG?
ECG is shown below. Many ECG readers will not comment any further on rhythm once ventricular pacing has been identified, but it is still critical to determine the atrial rhythm. Cardiology felt that there was baseline artifact and recommended immediate repeat ECG which is shown below. What do you think?
The patient needs a transvaginal ultrasound w/ doppler with gynecology consult and possible laparotomy TVUS is not just for torsion, it can also be used for ectopic pregnancies or pregnancy of unknown location Acute Ischemic Stroke Updates WITH Drs. The expanded window of 3-4.5 hours increased the NNT for a good outcome to 20.
A former resident texted me this ECG, done for epigastric pain in an 18 year old. I put it on Facebook EKG club and this is the response: No one knew for certain what that was, but Ken Grauer suspected artifact (due to lead placement over an artery) or a Crochetage sign, which is strongly associated with atrial septal defect.
Does that normal troponin and ECG obviate the need for cardiology consultation for my patient with a concerning story for acute coronary syndrome? The “bundling” heuristic—if I send a troponin, then an ECG is needed. Should I draw a venous or arterial blood gas before deciding on intubation?
morbidity and mortality - quality improvement - research grand rounds - r1 clinical knowledge: pres/rcvs - r4 case follow-up: compartment syndrome Morbidity and Mortality WITH dr. finney Takotsubo Cardiomyopathy with COVID-19 Increasing incidence of Takotsubo Cardiomyopathy with the COVID-19 pandemic Morbidity and mortality is similar to that of ACS (..)
This patient presented with weakness, decreased urine output, and vomiting: What is the ECG diagnosis? Here was a repeat ECG: QTc 523. The value of recognizing this particular ECG pattern — is that it may expedite your clinical diagnosis even before laboratory results return. This is pathognomonic for hypocalcemia.
In brief, the trial compared apixaban vs aspirin in patients who had had a stroke of unknown source and evidence of atrial cardiopathy. Recurrent stroke (the primary endpoint) occurred in 40 patients in each group. Apixaban did not reduce the rate of recurrent stroke over aspirin in these patients. The hazard ratio was 1.00.
His vital signs are all normal and the ECG done at triage does not show an occlusive myocardial infarction. Symptoms may include more severe chest pain radiating to the back, loss of consciousness, or symptoms of stroke if the blood supply to the brain is affected. It is described as a ripping sensation that radiates to his back.
Morbidity & MOrtality - Mini Lit Blitz - Post-Rosc Care - Qi/KT Morbidity & Mortality WITH Dr. Yates Case 1: Stroke and Stroke Mimics Early diagnosis of stroke improves stroke outcomes, where misdiagnosis is associated with an upwards of 4-time higher likelihood of mortality Missed strokes most often occur with atypical symptoms, in younger (..)
ECG, CXR, and troponin are negative. Notoriously elusive, with a high misdiagnosis rate, thoracic aortic dissection (AD) can mimic many conditions, including acute coronary syndrome (ACS, the most common), gastroesophageal reflux disease (GERD), stroke, and spinal-cord compression. ECG, CXR, and troponin are all normal.
Here is the ECG: The computer reads a long QT at 449 ms, and a Hodges QTc of 506 ms. From EMCrit: Taking control of severe hyponatremia with DDAVP An ECG recorded 2 days later with a K of 4.1: Figure-1: Both ECGs that were done in this case ( See text ). This patient presented with status epilepticus. What do you think?
Here is his ECG. See this articles: Heart Failure with Preserved Ejection Fraction (NEJM review) One etiology of LVH on the ECG is Hypertrophic Cardiolmyopathy (HOCM), and sometimes ECGs in patients with HOCM are specific for HOCM. But this ECG is NOT specific for HOCM. Figure-1: The ECG in today's case.
An ECG was recorded quickly on return to the ED: (sorry for poor quality, cannot get originals) What do you think? They called their transfer center cardiologist on call, who reviewed the case on the phone with them, as well as the ECG. In my opinion this makes the flutter waves slightly easier to recognize in this ECG.
In accordance with the last case (in which the patient presented only with vomiting and diarrhea), an ECG was recorded : (Figure 1) Someone thought this was slow VT with a "northwest" axis (towards aVR, or -135 degrees), but there are definite P-waves (with a long PR interval). But in the above ECG, V5 and V6 only have a Q-wave.
Laboratory Data CBC , CMP , EKG , and Troponins were normal. The two main causes of internuclear ophthalmoplegia are demyelination of the medial longitudinal fasciculus (MLF) from multiple sclerosis (MS) and ischemic cranial nerve damage from stroke. There were no oligoclonal bands.
Written by Bobby Nicholson MD, with edits by Meyers A woman in her 50s with past medical history of heart failure, prior stroke, atrial fibrillation on Eliquis, lung cancer in remission, and CKD, presented to the emergency department for evaluation of cough and shortness of breath. EKG was obtained in triage and read as ventricular bigeminy.
She has no previous cardiac history of which she is aware 911 was called and here is her Prehospital ECG: What do you think? link] Case continued She arrived in the ED and here is the first ED ECG. In comparison with the first ECG, I would guess that the artery is reperfusing. Stroke-volume:50 ml. Normal wall thickness.
Also think about NCSE in patients with prior cerebral pathology (ie, ischemic stroke); a patient who was seizing, was treated, and is not coming out of their post ictal state; and in patients with unexplained altered mental status with no other cause. Official diagnosis requires EEG, which is not something we can typically obtain in the ED.
Then I looked into the patient's chart and found an old EKG: This shows a previous QR-wave in V2, diagnostic of old anterior MI. I wrote back: "I am looking at his old EKG. He had a h/o ischemic cardiomyopathy and right MCA stroke. The cath lab had been activated and then they sent me the ECG. Cath lab was cancelled.
” “… but you could have a stroke or heart failure if you don’t get to the right place, so let’s get an EKG to confirm.” I was ecstatic to tell her the good news, “You do not have a rheumatologic condition!”
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