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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?
The ECG in Figure-1 was obtained from an 18-year old woman — who moments before been resuscitated from out-of-hospital cardiac arrest. How would YOU interpret her post-resuscitation ECG? Does this ECG in Figure-1 provide clue(s) to the etiology of this patient's cardiac arrest? QUESTIONS: In light of the above clinical history.
” Yes, I have seen clerking look like this and I can confirm, it does not go down well. Unless you’re documenting something hilarious, please keep it brief and to the point. History of Presenting Complaint In this section use SOCRATES to document the pain.
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.
The ECG and long lead II rhythm strip in Figure-1 — was obtained from a COVID positive patient with persistent tachycardia not responding to Diltiazem. Figure-1: The initial ECG — obtained from a patient with persistent tachycardia. ( To improve visualization — I've digitized the original ECG using PMcardio ).
EKG on arrival to the ED is shown below: What do you think? The providers documented concern for ST elevation in the precordial and lateral leads as well as a concern for hyperkalemic T waves in the setting of succinylcholine administration. 2) There was no terminal QRS distortion on these ECGs. or basilar ischemia.
The documentation does not describe any additional details of the history. 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.
This ECG was texted to me with no other information. The first ECG was recorded at 53 minutes after pain onset. The pain began to improve and this ECG was recorded: T-waves are not quite as tall, though still have a large AUC. An old ECG was found: As you can see, this patient has zero baseline STE, and normal T-waves.
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. Another ECG was recorded after the nitroglycerine and now without pain: All findings are resolved. No other symptoms.
She is well appearing, and while being placed on the monitor becomes anxious stating the symptoms are recurring. An ECG is performed and is shown below: Figure 1. Adapted from Dr. Smith’s EKG Blog. Another ECG is obtained and shown below. If the response is appropriate, get another EKG and assess the QT interval.
I have often written about how an ECG interpreted as "normal" by a conventional algorithm may well be manifesting OMI, or even long QT or hyperkalemia. Shifa Karim and Gabe Keller helped with a project to assess all these ECGs with the Queen of Hearts. The ECG told the story. I wanted to show some of the cases here.
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.
Add into this that the majority of children will be in normal sinus rhythm (NSR) by the time of assessment so to truly identify those who have something wrong we have to be confident in identifying arrhythmias where they are present and critical when analysing an ECG in NSR. All were examined and 98% had an ECG. Family history.
Physical exam reveals a well-appearing female in no acute distress. Her presenting EKG is shown below. Clinical features Patients often present after an episode of sudden syncope, although Brugada syndrome can also be found on a routine EKG. ECG to evaluate for arrhythmia. Neurological exam is also unremarkable.
Here are his EMS ECGs along with the Queen of Hearts interpretations below each one: EMS1 0650 EMS2 0707 Click here to sign up for Queen of Hearts Access The ECGs show RBBB and LAFB, with small but important concordant STE in V2. In EMS2 ECG, the T waves in V5 is possibly hyperacute. So the cath lab was activated.
An Initial ECG was performed: Initial ECG: Sinus tachycardia with prolonged QT interval (QTc of 534 ms by Bazett). A repeat ECG was performed 2 hours after arrival: QTc prolongation ato 722 ms now with alternating T wave pattern (T wave alternans) I texted this to Smith who responded: “T wave alternans and long QT.
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! The culprit mid LAD lesion was stented.
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. He had no previously documented medical problems except polysubstance use. 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. What are we seeing here?
During initial assessment, an ECG was obtained and revealed ST-segment elevation (STE) in the inferior leads with ST depression anteriorly. Initial ECG demonstrating inferolateral ST segment elevation and anteroseptal depression, just prior to cardiac arrest. The ECG showed ST-segment elevation without obstructive coronary disease.
Well, that can be a problem. Sometimes things we do are well grounded in evidence. Things like reading ECGs, echocardiograms, as well as learning to do procedures. Well, do you know the actual trials underpinning this evidence? They sit in a Google document. It will be a working document.
The following ECG was obtained. Note that the machine read is "normal sinus rhythm, normal ECG." ECG 1 What do you think? I sent this ECG to Dr. Smith and Dr. Meyers with no clinical context. Smith comment: this troponin alone should be enough data to activate the cath lab, regardless of the ECG. <0.049 ng/mL).
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.
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. Pretest probability: Even before the ECG, a patient with a history of coronary stent has a 90% chance that his wide complex tachycardia is VT.
An ECG was performed in the ED at 1554: Original image unavailable, this is the only recorded scanned ECG available. In a patient with syncope and fever, this ECG looks more like Brugada. Smith comment: the ECG in question could be due to Brugada, even though there is a change from baseline. PM Cardio digitized version.
His ECG is shown: What do you think? The history thus far is highly suggestive of OMI, so we must study the ECG very closely to see if we can confirm this. The Queen of Hearts does not care about rhythm analysis, she simply looks at the ECG and decides whether it represents OMI or not. He pointed out the precordial swirl sign.
In this study, they found that prone positioning resulted in significant improvement in oxygenation, as well as a 50% decrease in mortality at 28 days (Guerin et. Remove ECG leads and patches. Reattach EKG leads to back. Document thorough skin assessment every nursing shift, and inspect weight-bearing ventral surfaces.
I remember Allie well from her days in the Research volunteer program at Hennepin. An initial EKG was obtained: Computer read: sinus tachycardia, early acute anterior infarct. Here is her prior EKG: When compared to the old EKG – Q waves present before, TWI in aVR present before, but all other changes are new.
Below is the first ECG, signed off by the over-reading cardiologist agreeing with the computer interpretation: ST elevation, consider early repolarization, pericarditis, or injury. Emergency physician: STEMI neg but with elevated troponin = Non-STEMI The first ECG was signed off. Repeat blood work and ECG 0845: repeat trop over 7000.
Alkali burns result in liquefaction necrosis, allowing for deeper tissue injury as well as vascular injury that can lead to both local and systemic toxicity [1]. Circulation Assess heart rate, blood pressure, peripheral and central CRT, pulses and 3 lead ECG. Establish IV access and begin fluid resuscitation with 250ml boluses of 0.9%
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. I labeled ECG. His chest was tender.
Sean Rees MD, written by Pendell Meyers, other case by Sam Ghali and Steve Smith Take a look at these two ECGs below from two patients in the ED, first without any clinical context. 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)?
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.
Queen: #1: NOT OMI, HIGH CONFIDENCE Queen: #2: NOT OMI, HIGH CONFIDENCE ECG 1 Interpretation: there is terminal T-wave in V3-V6. See 2 dozen examples here: Understanding this pathognomonic ECG would have greatly benefitted the patient. And ECGs can change and evolve even when there is no ischemia. Is this Wellens' pattern A?
Here is his initial ECG: What do you think? Although diagnostic of MI, it is highly suspicious for " Old inferior MI with persistent ST Elevation" or "inferior aneurysm morphology" because of the well-formed Q-waves and the flat T-waves. The patient's chest pain had resolved by the time of the ECG 2. The T-waves are flat.
Here is her prior baseline ECG (first), and her ED ECG (second): Baseline: ED ECG: What do you think? Do you agree with the computer's interpretation of "Normal ECG"? The ECG shows sinus rhythm with normal QRS and R wave progression. This ECG clearly meets STEMI criteria by the way, regardless of age or gender.
It radiated to both shoulders and both upper extremities, and there was shortness of breath and diaphoresis as well. Triage ECG (no prior for comparison): Computer algorithm read: "Sinus rhythm, low voltage QRS, inferior myocardial infarction, probably old." Every note says "no ischemic changes on ECG." Day 2: No ECGs recorded.
At 3:55 AM during that kind of a night shift, this ECG (among many others) was brought from triage for review by my team. We knew only that the ECG belonged to a man in his 50s with chest pain and normal vitals. Here is the computer interpretation: So we have a triage-computer-normal ECG. No prior available.
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?
This ECG was texted to me in real time, but I did not notice the message until about an hour after it came. "50 This was my response: "This looks like a worrisome EKG. But by now you must have a repeat ECG. But by now you must have a repeat ECG. Another ECG was recorded while waiting for the cath team (it was nighttime).
Here is the first ED ECG, with no pain: Sinus rhythm. The ECG in the chart was read as "no obvious ST changes," (even though no previous ECG was available) and the formal read by the emergency physicians was: "ST deviation and moderated T-wave abnormality, consider lateral ischemia." Computerized QTc = 419. It was stented.
” Yes, I have seen clerking look like this and I can confirm, it does not go down well. Unless you’re documenting something hilarious, please keep it brief and to the point. History of Presenting Complaint In this section use SOCRATES to document the pain.
Currently, the infusion of IV calcium before diltiazem is not well understood, and more studies have focused on administering IV calcium prior to verapamil than diltiazem. Patients confirmed on ECG to have atrial fibrillation or atrial flutter Patients with HR >120 bpm. Article: Rossi N et al.
Here is her 12-Lead ECG: There’s a sinus rhythm at around 70 bpm. It is difficult to answer this question based on this single ECG alone. We don’t see excessive ST Elevations (“Tombstones”) that would suggest acute STEMI, but clearly acute STEMI can certainly present with moderate ST Elevation as well.
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