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The ECG in Figure-1 was obtained from a previously healthy man in his early 20s — who initially presented with GI symptoms, that then evolved into CP ( C hest P ain ). QUESTIONS: Given the above history — How would YOU interpret the initial ECG that is shown in Figure-1 ? Figure-1: The initial ECG in today's case. (
Electrocardiograms (EKGs) are at the top of modern healthcare as indispensable diagnostic tools for identifying arrhythmias, heart attacks, and other cardiac disorders. In this blog, we delve into the power of EKG training, the essential skills healthcare professionals need, and strategies to excel in using this life-saving technology.
This is another case sent by the undergraduate (who is applying to med school) who works as an EKG tech. How is it possible that a kid who has not even started medical school can know so much about EKGs and cardiology? He had an EKG taken at the clinic: What do you think? Normal EKG”. Normal ECG.
Written by Jesse McLaren A 50 year old presented to triage with one hour of chest pain, and the following ECG labeled normal by the computer (GE Marquette SL) algorithm. see reference below) Whats the gold standard for ECG interpretation: is it cardiologist interpretation? What do you think? The latest is Langlois-Carbonneau et al.
The way to get good at it is to see a lot of them, and also see a lot of fake HATWs (mimics) Here is a difficult pair of ECGs that demonstrate a difference: One ECG is normal variant STE. The more abnormal leads and lead areas you can identify in a given ECG — the more solid the evidence of acute OMI becomes. Which is which?
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 ).
This is another case sent by the undergraduate (who is applying to med school) who works as an EKG tech. He was admitted to the hospital for evaluation of these symptoms — but no ECG was done at that time. This EKG is very subtle, but it is diagnostic of LAD occlusion. The Queen of Hearts does not see the hyperacute T waves.
Willy is a cardiology fellow with a keen interest in the ECG in OMI. If an immediate EKG was obtained, it was not saved in the medical record. The first available EKG was recorded just after midnight, presumably around the time the result of the troponin came to clinical attention. The patient said, "I just don't feel good."
Below is the triage ECG, with a computer interpretation (Marquette 12 SL) of “normal” which was confirmed by the over-reading cardiologist. Should this patient continue to stay in the waiting room, without interruption of the physician to interpret the ECG, because the computer interpretation is normal? What do you think?
Here is his initial ECG around 1330: What do you think? The ECG shows sinus tachycardia with RBBB and LAFB, without clear additional superimposed signs of ischemia. Initial high sensitivity troponin I: 3,830 ng/L (URL 20 ng/L for men) 1445: Similar to initial ECG. He was intubated for altered mental status.
Below are serial ECGs focusing on the inferior leads and aVL. First, what’s the interpretation of each ECG on its own? #1 2 Normal ECG #3. 2 Normal ECG #3. But 90 minutes later troponin returned at 70ng/L (normal <26 in males and <16 in females), and a repeat ECG was done (ECG#2) for recurring chest pain.
EKG from triage: Here is his previous ECG: Normal ST Elevation Resident's interpretation: Reperfusion pattern/Wellens' with biphasic T waves in V2 and V3, and in comparison to an EKG in 2020 this is new. Repeat EKG: Resident interpretation: ST elevation in V2 significantly different than his previous EKG.
The patient with no prior cardiac history presented in the middle of the night with acute chest pain, and had this ECG recorded during active pain: I did not see any ischemia on this electrocardiogram. I think the ECG is normal. OMI is a clinical diagnosis that includes the ECG. This is a case I had quite a while back.
Written by Jesse McLaren Three patients presented with acute chest pain and ECGs that were labeled by the computer as completely normal, and which was confirmed by the final cardiology interpretation (which is blinded to patient outcome) also as completely normal. It is well known that NOMI usually has a normal ECG or nonspecific ECG.
We will update this post if we receive information about her outcome. ECG Number 1, 11:57 a.m.: There is a wide-complex tachycardia at a rate of about 230 bpm. This photo shows an ECG that is not lying flat, so it is difficult to line up the complexes. She was alert and oriented. Her BP was reported as being “stable”.
Don't miss his analysis and assessment of the Queen of Hearts AI OMI ECG bot -- that assessment is at the very bottom of the post. Here is her ED EKG: What do you think? I would have very high suspicion for OMI on this ECG. Past medical history included Crohn’s disease, hyperlipidemia, hypothyroidism, and she smoked 1ppd.
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.
This case comes from Jason Winter, of The Facebook Clinical Electrocardiology ECG Page. Here is her first prehospital ECG: What do you think? However, again, the formula was developed only in ECGs with at lead 1 mm of STE in V2 and V3, so does it apply? Serial ECGs improve the sensitivity of ST elevation on the ECG for MI.
She had an ECG recorded at triage: What do you think? What was the outcome?" No Previous ECGs Available. But she does label V2 as "OMI High Confidence" and V1 as "OMI Low confidence" Like good physicians, they recorded another ECG at 10 min: What do you think? Learning Points: Serial ECGs are critical.
Written by Magnus Nossen with Edits by Grauer and Smith The ECGs in today’s case are from 3 different patients all presenting with new-onset CP ( Chest Pain ). All ECGs were recorded by EMS, and transferred to a PCI capable center for evaluation. For 2 of the 3 patients — the cath lab was activated based on the ECG.
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 his first prehospital ECG: 1st Prehospital ECG What do you think?
This is a "classic" ECG of very good quality for you to use in a classroom setting. The ECG: This ECG could be considered "classic" for an inferior wall ST elevation M.I. The ECG: This ECG could be considered "classic" for an inferior wall ST elevation M.I. He is pale, cool, and diaphoretic.
Here is his initial ED ECG: What do you think? I read this ECG without any history as reperfusing inferior and posterior OMI due to the Q-wave in lead III with minimal STE and reciprocal ST depression in V2-V4 (which should never be there). We send each other EKG by the dozens every day. Most are OMI look alikes (mimics).
This is the result for this ECG, from MDcalc.com : The most accurate cutpoint is 18.2. Outcome: 100% LAD Occlusion Here the Queen explains why: The dark blue tells us that she is looking especially at the QRS in V3 and the T-wave in V2 and V3. Here is a similar case from Pendell: This ECG was handed over at triage.
Both cases had an EMS ECG that was transmitted to the ED physician asking "should we activate the cath lab?" On arrival to the ED, while waiting for cath lab team, he obtained another ECG: You can now see the full voltage of the high-voltage QRS, likely with some degree of LVH. Serial ECGs remained unchanged. What do you think?
Here is his presenting ECG: ECG 1, t = 0 What do you think? His transfer packet included notes, labs, cath report, and ECG reports, but no actual ECG images. Smith's ECG Blog. When he reviewed the case, he only had access to the accepting facility ECG. He did not have access to ECG 1.
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.
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.
I received the following text message with these 3 EKGs (providers text me ECGs all day every day; most are false positives; many are subtle true positives): "Hi Steve, here are 3 EKGs for you (my colleague's case). Opiates are associated with worse outcomes in Myocardial Infarction. Cath attending is aware. Am Heart J.
Alcohol withdrawal syndrome: improving outcomes through early identification and aggressive treatment strategies. fold higher risk of NSTI than the control group 12 For those without comorbidities , AUD exhibited a 15.2-fold fold higher risk of NSTI than the control group 12 For those without comorbidities , AUD exhibited a 15.2-fold
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.
EMS arrived and recorded this ECG: What do you think? See same ECG below with computer automated interpretation, using the Glasgow ECG algorithm which apparently is used by many different providers and devices Amazing that the computer calls this normal. Next day ECG. And yet it still says "normal". Learning Points: 1.
Here was his triage ECG: What do you think? I sent this ECG to the Queen of Hearts (PMcardio OMI), and here is the verdict: You can subscribe for news and early access (via participating in our studies) to the Queen of Hearts here: [link] queen-form Then I learned that a Code STEMI was activated for concern of anterior "STEMI" in V1-V2.
Here is his ECG at triage: What do you think? See this post if you dont know that pattern yet: Precordial Swirl -- 20 cases of Swirl or Look-Alikes Here was a repeat ECG done within 20 minutes (still with ongoing pain): It still looks like active OMI to me, but perhaps slightly improved from the first one. Outcome of case 2?
Automatic detection of cardiac conditions from photos of electrocardiogram captured by smartphones by Wong et al Topic: The use of smartphone technology in interpreting ECGsOutcome rating: Worth a peek Machine-learning algorithms for ECG interpretation are rapidly improving in accuracy.
The below ECG was recorded. The ECG does not show any definite signs of ischemia. In fact, the ECG was described as normal, and without serial ECGs or prior ECGs for comparison it could be. PEARL: Increased vagal tone is highly likely to be the cause of the abnormal rhythm in ECG #2.
Post-ROSC management is nuanced and challenging but helps to ensure good outcomes. In theory, rapid identification of the underlying cause should improve outcomes by allowing clinicians to tailor management. Diagnostic yield, safety, and outcomes of Head-to-pelvis sudden death CT imaging in post arrest care: The CT FIRST cohort study.
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!
Wolf-Parkison-White Syndrome (WPW) Case Question: What are the characteristic ECG findings of this condition and how is this condition managed? These particular EKG findings define a “Wolff-Parkinson-White Pattern.” WPW Syndrome consists of characteristic EKG findings as well as symptomatic arrhythmias. Crit Care Nurse.
His initial EKG is the following: What do you think? Gorgels et al (5) looked at procainamide vs lidocaine and again and primary outcome was VTach termination. If procainamide is utilized, a baseline EKG should be obtained to assess the QRS and QTc at baseline. Learning that we can be calling lidocaine Lignocaine from now on.
The minute this medical student saw the first ECG, he knew the diagnosis without any further information. Reading ECGs is hard, but can be done with commitment to learning, which comes from an awareness of its importance. You need to be interested and understand the value of the ECG. She had this ECG recorded: ECG 1: QTc is 484.
Which had the more severe chest pain at the time of the ECG? Patient 2 at the bottom with a very subtle OMI complained of 10/10 chest pain at the time the ECG was recorded. And as we have shown before, morphine leads to slower times to treatment and worse outcomes. 2 middle aged males presented with chest pain.
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.
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. Long term outcome is unavailable.
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