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Bedside cardiac ultrasound showed moderately decreased LV function. She had an ECG recorded: This is left bundle branch block (LBBB), with appropriate proportional discordance. Here is one of the strips This is clearly polymorphic VT and probably torsade de pointes Subsequent ECGs. She was intubated. No wall motion abnormality.
This was sent by an undergraduate (not yet in medical school, but applying now) who works as an ED technician (records all EKGs, helps with procedures, takes vital signs) and who reads this blog regularly. The undergraduate's analysis: This EKG shows J point elevation of about 0.5-1 Edited by Smith He also sent me this great case.
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. The patient arrived just after 10 AM, and the following EKG was obtained. There are no further EKGs or troponin measurements.
Pain improved to 1/10 after EMS administers 324 mg aspirin and the following EKG is obtained at triage. If this EKG were handed to you to screen from triage without any clinical information, what would you think? Do you appreciate any dynamic changes compared to the patient’s prior EKG? What do you think? In fact, Kosuge et al.
He had active chest pain at the time of triage at 0137 at night, with this triage ECG: What do you think? I sent this ECG, without any text at all, to Dr. Smith, and he replied: "LAD OMI with low certainty. Back to the case: Unfortunately, the ECG was not understood by the provider. V3 is the one that is convincing."
Here is his ED ECG at triage: Obvious high lateral OMI that does not quite meet STEMI criteria. He had a previous ECG on file: Proving the findings are new The cath lab was activated. Bedside cardiac ultrasound with no obvious wall motion abnormalities. Bedside cardiac ultrasound with no obvious wall motion abnormalities.
The following ECG was obtained. ECG 1 What do you think? The ECG shows sinus bradycardia but is otherwise normal. There is TWI in lead III, but this can be seen in normal ECGs. The following ECG was obtained around midnight. The machine read was "Normal sinus rhythm, normal ECG." ECG 2 What do you think?
All initial ECGs were labeled ‘normal’ or ‘otherwise normal’ by the computer interpretation, and below are the ECGs with the final cardiology interpretation. 1-3] But these studies were very short duration and used cardiology interpretation of ECGs or emergent angiography rather than patient outcomes.
Her ECG is shown below: What do you think? The conventional machine algorithm interpreted this ECG as STEMI. Alternatively, with STE in V1 and III, and STD in I and aVL, this ECG could represent proximal RCA OMI with right ventricular involvement. What do you do clinically when the ECG looks like this?
” Yes, I have seen clerking look like this and I can confirm, it does not go down well. Examples of examination findings you might find helpful to keep in mind (list not exhaustive): GCS 15/15- alert, orientated, looks comfortable, warm and well perfused, in obvious pain, looks pale and clammy etc.
This ECG was recorded in triage. The computer interpretation is: “Sinus Brady with moderate intraventricular conduction delay, nonspecific t wave abnormality, abnormal EKG” What do you think? Case Continued The ECG findings were not recognized. Therefore, no matter the initial ECG, record serial ECGs.
Here is his first ECG (1/10 pain): Smith: sinus rhythm with RBBB and normal ST-T. An ECG from 4 years prior was the same. In the absence of clear ECG signs of OMI, one should always start with aspirin and NTG, perhaps intravenous NTG, and see if the pain can be managed. He presented on this day because it did not go away.
Here is the initial ECG at 13:17 with no prior ECG in the patient’s chart for comparison: What do you think? This is another version of the same ECG, lower quality, and with an additional filter applied. See Ken Grauer's additional comments about this ECG at the end of the post!
I was texted this ECG just as I was getting into bed. Ken (below) is appropriately worried about pulmonary embolism from the ECG. What I had not told him before he made that judgement is that the patient also had ultrasound B-lines of pulmonary edema. Figure-1: I've labeled the initial ECG in today's case.
Does that normal troponin and ECG obviate the need for cardiology consultation for my patient with a concerning story for acute coronary syndrome? 4 However, emergency physicians rely on gestalt to predict outcomes well. The “bundling” heuristic—if I send a troponin, then an ECG is needed. Urology took him for orchiopexy.
The below ECG was recorded. The ECG shows obvious STEMI(+) OMI due to probable proximal LAD occlusion. This ECG does not have the typical ST-vector of an LAD occlusion. See below for Ken Grauer Comment on the initial ECG: == On arrival, another ECG was recorded: There appears to have been quite a bit of spontaneous reperfusion!
These diagnoses were not found in his medical records nor even a baseline ECG. An ECG was obtained shortly after arrival: What do you think? There is no evidence of WPW on this ECG, but it is diagnostic for OMI. He reported a history of “Wolf-Parkinson-White” and “heart attack” but said neither had been treated.
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 RV is supplied during systole as well as diastole.
Her heart rate was very fast, so we obtained an ECG immediately: ECG: What do you think? That would likely slow the ventricular rate as well, but would have a higher likilihood of converting to sinus. WHY Did We Think Today's ECG was Supraventricular? As a result — We can not rule out VT on the basis of this single ECG.
Initial ED ECG: What do you think? Then we must consider clinical data other than the ECG, for a pretest probability : Of all wide complex tachydysrhythmias, the majority are VT. Pads were placed with ultrasound guidance, so they were in the correct position. Definitive diagnosis that ECG #1 is in fact VT is more than academic.
The plan was that she would get a two-week, continuous EKG monitor placed and have a sleep study at this hospital. “Well, this isn’t really the aspect of my specialty that I specialize in.” She follows up at a “highly ranked” west coast academic medical center, near where she lives half the year.
He arrived in the ED and had an immediate bedside cardiac ultrasound while this ECG was being recorded. The bedside ultrasound (video not available) reportedly showed only a slightly reduced LV function. Here is the ECG: What do you think? Here is the post cardioversion ECG: What do you think?
Initial ROSC was obtained, during which this ECG was obtained: What do you think? In addition to all of the above, there are T wave inversions in III and aVF, as well as T wave inversions in V2-V4. When the ECG differential is between OMI on the one hand, and PE/type II OMI on the other, the absence of VT/VF strongly favors PE.
Colin is an emergency medicine resident beginning his critical care fellowship in the summer with a strong interest in the role of ECG in critical care and OMI. An ECG was obtained shortly after arrival: ECG 1 What do you think? The ECG has a lot of artifact, and the amplitude is very small, making interpretation challenging.
He had this ECG recorded. He was rushed by residents into our critical care room with a diagnosis of STEMI, and they handed me this ECG: There is sinus tachycardia with ST elevation in II, III, and aVF, as well as V4-V6. But, remember, we do not evaluate and treat ECGs, we evaluate and treat patients. Are the lungs clear?
Over some time and the pain moved into her other arm as well as her jaw. 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. She said this was midsternal and felt like a tightness.
We will start with his baseline EKG: There is voltage suggestive of LVH. This is his presenting EKG (T= 26min): What do you think? Hence, the term "pseudonormalization", because it is not really normal - LVH should have repolarization changes seen in the baseline EKG. Thus, there is relative ST depression.
Here is the prehospital ECG at 1935: Sinus rhythm with left bundle branch block (LBBB). In Sgarbossa's study, just 1 mm concordant STE in just 1 lead was 92% specific for MI and earned the ECG 5 points. Just 1 mm concordant ST depression in just 1 lead of V1-V3 was 96% specific for MI and would earn the ECG 3 points.
Point-of-Care-Ultrasound (POCUS) is a bedside modality that can assist Emergency Physicians (EPs) in differentiating PE from other causes of cardiac arrest. Multiorgan POCUS The diagnostic power of POCUS often resides in combining multiple ultrasound exams. 1-3 As many as 25% of acute PE cases present as sudden cardiac death.
Here is his ECG: Original image, suboptimal quality Quality improved with PM Cardio digitization The ECG is highly suggestive of acute right heart strain, with sinus tachycardia, S1Q3T3, and T wave inversions in anterior and inferior with morphology consistent with acute right heart strain. Moreover, there is tachycardia.
Her presenting ECG is shown below: ECG 1 What do you think? I had previously run this ECG through QOH in the PMcardio app environment and she reported mid confidence, shown below. You can see that version 2 has a higher number than version 1, hence she sees the ECG as more OMI-like than version 1. I sent this to Drs.
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. Our first 12 lead ECG was then recorded at 0926. What do you think?
A bedside cardiac ultrasound was normal. An ECG was recorded: Avinash was understandably confused by this ECG. He wrote: "ECG 1 - shows wide ???IVCD It appears to be benign in children as well (see references below). I sent it to my friend, Ken Grauer , who is very meticulous in his ECG reading.
The ECG told the story. EMS recorded these prehospital ECGs: Time 0: In V2-V4, there is ST elevation that does not meet STEMI "criteria," of 1.5 Time = 24 min S-wave depth is diminishing These prehospital ECGs were lost and not seen. This patient has a non-diagnostic ECG by most rules. She called 911. STE 60 V3 = 1.5
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.
She denied chest pain and denied feeling any palpitations, even during her triage ECG: What do you think? She was awake, alert, well perfused, with normal mental status and overall unremarkable physical exam except for a regular tachycardia, possible rales at both bases, some mild RUQ abdominal tenderness. And another example.
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.
Tachycardia may be present both from many medications or drugs, as well as withdrawal. Glucose POC ECG: Is this actually sinus tachycardia? Looking at the initial or even repeating the ECG will be helpful here. Let’s use the example of the well appearing patient, without significant comorbidities. Do they have edema?
Clinical pathologic case presentation - r1 diagnostics/therapeutics: Lumbar punctures - AIRWAY GROUND ROUNDS- r4 capstone - r3 taming the sru - ultrasound grand rounds Clinical pathologic case presentation WITH Drs. If assessing for SAH, xanthochromia may not appear until 12 hours after onset, though may appear after 2-4 hours.
EMS recorded these ECGs: Time 0: In V2-V4, there is ST elevation that does not meet STEMI "criteria," of 1.5 The pain completely resolved after nitroglycerine Moments later, the this ECG was recorded in the ED when she had been pain free for moments only: Computer read: Normal ECG. E EKG: a negative ECG (score = 0) 3.
ULTRASOUND GOODIE BAG ULTRASOUND FOR LATE PREGNANCY [PODCAST]: While not a routine exam we perform other than confirming fetal heart tones, definitely some great pearls on more advanced US topic. Consider an ultrasound guided ulnar nerve block. Well, this may not be completely true. Part 1 here.
A 40 something woman with a history of hyperlipidemia and additional risk factors including a smoking history presented with substernal chest pain radiating to "both axilla" as well as the upper back. The initial tracing (EKG 1) was obtained. Clinician and EKG machine read of acute pericarditis. What do you think?
An immediate 12-lead EKG was obtained: There is ST elevation in leads aVR and V1, with marked ST depression in I, II, III, aVF, V3-V6. Smith comment: This patient did not have a bedside ultrasound. The ECG cannot diagnose the etiology of ischemia; it only the presence of ischemia, from whatever etiology. What should be done?
ULTRASOUND IN CHEST PAIN: [BLOG]: It is never a bad idea to throw an ultrasound probe on your patient with chest pain. More FOAMed HARDWARE MALFUNCTION PACEMAKER AND AICD MANAGEMENT IN THE ED [BLOG]: EM Docs brings us some well needed cardiac hardware meducation on the patient with AICD/pacemaker issues presenting to the ED.
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