EXTRA COPY — ECG Blog #531: WCT: What to Do? — EXTRA COPY

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Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

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for LBBB conduction/morphology

See ECG Blog #204 (video, pdf, etc)

https://ecg-interpretation.blogspot.com/2021/03/ecg-blog-204-ecg-mp-22-bundle-branch.html

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ECG Blog #287 — working thru Dx of AFlutter (audio, pdf, lewis leads)

https://ecg-interpretation.blogspot.com/2022/02/ecg-blog-287-sinus-tach-with-st.html

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The November 12, 2019 post in Dr. Smith's ECG Blog — in which I review my approach to a Regular SVT rhythm.

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PEARL #4: The method that I favor to try first — is to simply LOOK for flutter waves! The diagnosis of AFlutter can be established in a regular SVT at ~150/minute — IF you are able to identify regular atrial activity at ~300/minute. Nothing else results in regular atrial activity at this fast of a rate (Atrial tachycardia will rarely be faster than 250/minute ...).

• The way in which I look for flutter waves is to carefully set my calipers at precisely HALF the R-R interval of the regular SVT (since IF the rhythm is AFlutter — then the atrial rate should be twice the ventricular rate if there is 2:1 AV conduction). The short RED lines in leads II and aVF of Figure-2 confirm that there is indeed 2:1 atrial activity in this tracing — which tells us even before application of a vagal maneuver or administration of Adenosine (or other AV blocker) that the rhythm is virtually certain to be AFlutter.
• 
  
• PEARL #5: My usual "GO TO" leads for identifying atrial activity are i) Lead II — which is typically the BEST lead for identifying atrial activity. In AFlutter — leads III and aVF also usually provide ready evidence of 2:1 atrial activity; ii) Lead V1 — Next to lead II, lead V1 is often the 2nd-best lead in my experience for identifying atrial activity. With AFlutter — one will often see small amplitude positive deflections of AFlutter in this V1 lead; iii) Lead aVR is often surprisingly helpful for identifying atrial activity; and, iv) IF none of the above leads suggest atrial activity — then I’ll survey the remaining 7 leads as I look for atrial activity. That said, AFlutter will almost always provide ready evidence of atrial activity in one or more of my “Go To” leads.
• The reason the diagnosis of AFlutter is so subtle in today's case — is that except for leads II and aVF, flutter waves in other leads are almost perfectly hidden within the QRS complex!

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Acknowledgment: My appreciation to Sanooj Op (from Calicut, India) for making me aware of this case and allowing me to use this tracing.

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Relevant ECG Blog Posts to Today’s Post: 

• See ECG Blog #185 — for review of the Systematic Ps, Qs, 3R Approach to Rhythm Interpretation.
• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
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• ECG Blog #204 — Reviews a user-friendly approach to the ECG Diagnosis of conduction defects (ie, LBBB — RBBB — IVCD).
• 
  
• ECG Blog #287 — Working through the diagnosis of AFlutter (with Audio Pearls, PDF, Lewis Lead).
• The November 12, 2019 post in Dr. Smith's ECG Blog — in which I review my approach to a Regular SVT rhythm.

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O.p. Sanooj — FB Messenger (5-12.1-2026)

from Calicut, India — I am from Calicut, India. Myself Dr Sanooj Op

Sir..does the ecg show SVT? This patient is hemodynamically stable. If it is an SVT, I can give adenosine IV bolus. Otherwise I can give amiodarone. Am I right sir? Here the clinical dilemma is to differentiate

MY REPLY:

Great CASE! And your overall reasoning IS correct. But there are several things that need to be considered. #1) Is this your patient? If not — Is this from the internet? ( IF SO — Please ALWAYS give me the EXACT LINK to the post where this tracing is from so I can check it out and interact). #2) What this is (ie, SVT vs VT) often DEPENDS A LOT on the clinical situation (ie, Young otherwise healthy adult — in which case things like idiopathic VT (in which there is NO underlying heart disease) vs older adult with heart disease (in which case VT is much more likely). #3) It is important to ALWAYS first DESCRIBE what you see !!! This greatly narrows your differential diagnosis (ie, this is a regular WCT at ~150/minute without regular P waves). #4) Now go further — QRS morphology here is PERFECTLY CONSISTENT with LBBB conduction! All upright R in lateral leads I and V6 and predominantly negative in anterior leads with a VERY steep downslope = LBBB conduction is VERY likely — therefore this very likely is supraventricular — so if pt is stable and esp. if a younger adult without heart disease or an older adult with a history of SVT — I'd try Adenosine first. #5) Looking further and GETTING YOUR CALIPERS OUT — we see what looks like "spikes" midway thru the QRS which is probably atrial activity — but it is upright, so not retrograde — AND — my description of a regular rhythm at about 150/minute tells me to LOOK FOR FLUTTER — and my calipers can walk out perfect 2:1 atrial activity — so this is almost certain to be AFLUTTER — so I'd treat this for AFlutter. Adenosine would slow the rate temporarily but not convert the rhythm — so I'd probably try IV Amiodarone. So this is a GREAT case — If you could tell me what happened (and/or give me the link where the blog is from) — I'll contact the author and might want to use it for an ECG Blog (that I have just described for you how to assess this rhythm! —

MY REPLY:

Hi. I worked on the original figure that you sent — and I think it looks different enough from the original that no one will recognize where this comes from. So I with your permission — I want to go ahead and publish this as an ECG Blog, as it is an EXCELLENT CASE for others to learn from.

If you do have any follow-up — Please let me know — but I am confident enough that this is AFlutter with 2:1 AV conduction and LBBB conduction even without follow-up.

THANKS — :)

EXTRA COPY — ECG Blog #530: Old or New Wellens? — EXTRA COPY

I was sent the ECG in Figure-1 — but without the benefit of any history. I was asked for my opinion as to whether this tracing represented an acute STEMI? 

QUESTIONS:

• How should I answer? 
• Is this "new" or "old" Wellens?

Figure-1: The initial ECG in today's case — which was sent to me without the benefit of any history. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Answer:

Even without knowing the history — the ECG in Figure-1 is clearly of concern:

• PEARL #1: Although there is often a tendency to skip the basics, and go straight to the obvious findings (which are seen here in the inferior leads!) — I prefer to always take a brief look first at the rhythm. (For this — I favor the Ps,Qs,3R Approach for systematic rhythm interpretation = ECG Blog #185).
• To Emphasize: There is no need to spend more than a couple of seconds with this initial glance at the rhythm — and there is no need to come up with a definitive rhythm diagnosis at this point in time!
• Instead — You simply want to find out: i) What is the approximate Rate of the rhythm? (ie, Is the patient likely to be hemodynamically stable at this heart rate?); — and, ii) Is the rhythm sinus or something else?).

Is the Rhythm Sinus?

If I were charged with treating the patient in today’s case — I’d immediately go to the bedside to determine a brief history, and verify that this patient was hemodynamically stable with the rhythm shown in Figure-1. Since I was not yet provided with this information — I assumed the patient was stable enough for me to proceed with my interpretation of today’s initial ECG:

• PEARL #2: The rhythm is not sinus — because the P wave in lead II is not upright! ( = YELLOW arrows in the inferior leads in Figure-2). Assuming there is no lead reversal — the finding of a negative P wave in lead II indicates either a junctional or low atrial rhythm.
• Note that these negative P waves in lead II of Figure-2 do manifest a constant PR interval, such that they are conducting (because these P waves are Related by a fixed PR interval to neighboring QRS complexes).
• Note also that no P waves are seen throughout the long lead V1 rhythm strip at the bottom of the tracing. However, there is a negative P wave seen in simultaneously-recorded lead V3 (YELLOW arrow in that lead). Thus the reason no P wave is seen in lead V1 — is that morphology of the retrograde P wave in lead V1 must be isoelectric to the baseline.

Otherwise ... 

• The QRS complex is narrow ( = not more than half a large box in duration) — so the rhythm is supraventricular.
• The ventricular rhythm is Regular — at a Rate of ~50/minute (ie, R-R interval a tiny bit over 6 large boxes in duration).
• Bottom Line: Given lack of a visible P wave in lead V1 + the narrow QRS + the slow ventricular rate of ~50/minute — this appears to be a junctional escape rhythm.

Figure-2: Negative P waves in the inferior leads indicate this is a non-sinus rhythm. The narrow QRS, slow rate and lack of visible atrial activity in lead V1 suggest this is a junctional escape rhythm.

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The Rest of the ECG ...

In addition to the slow junctional escape rhythm — Figure-3 highlights KEY findings in the leads of most concern:

• Extremely large Q waves are seen in leads III and aVF. This is associated with a hyperacute appearance of the ST segment that manifests considerable J-point elevation with a straightened ascending ST segment takeoff. There is fairly deep terminal T wave inversion.
• The 3rd inferior lead ( = lead II) — manifests a bizarre, fragmented QRS, with similar looking but less marked ST-T wave changes.
• Reciprocal ST-T wave changes are seen in lead aVL (within the BLUE rectangle) — in the form of a straightened and depressed ST segment (that manifests gradual downsloping, but which finishes with terminal T wave positivity).
• Lead V3 is uninterpretable due to artifact ...
• Less marked but still concerning ST-T wave findings are present in 3 additional leads. These include: i) Lead I (which is similar in shape, but with less prominent reciprocal changes compared to aVL); ii) Lead V2 (which manifests ST segment straightening with loss of the normal slight ST elevation usually seen in this lead); — and, iii) Lead V6 (with a QRS and ST-T wave similar to that seen in lead II).

Putting It All Together:

I had more questions than answers after reviewing this ECG: 

• The extremely large Q waves in leads III and aVF indicate that the patient has had an inferior infarction at some point in time.
• The hyperacute-looking ST segments with ST elevation, in association with reciprocal ST depression in lead aVL — suggest an inferior MI that may be recent (or ongoing) — with the findings in leads V2 and V6 suggesting associated posterior and lateral involvement.
• The above said — the terminal T wave inversion in the inferior leads and in lead V6 + terminal T wave positivity in leads I,aVL and V2 could all represent evolving reperfusion changes of completed infarction.
• 
  
• BOTTOM Line: We need some history to proceed further with our interpretation. Along the way — finding a previous ECG for comparison should prove invaluable for determining what is "new" vs "old".

Figure-3: I've labeled the leads of most concern. 

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The CASE Continues:

I was finally able to learn a bit more about this case.

• This ECG is from a middle-aged woman with known coronary disease, having undergone stent placement following an MI about 1 year earlier.
• She presented this time with ongoing severe CP (Chest Pain) that began ~2 hours prior to the time that ECG #1 was recorded. 
• Despite the slow junctional escape rhythm — she was hemodynamically stable.

My Thoughts:

• Although with this past and present history I was still uncertain as to what was "new" vs "old" vs "new superimposed on old" — given the presence of hyperacute-looking ST-T wave changes with ST elevation and ongoing severe CP — prompt cath is needed to define the anatomy!
• 
  
• PEARL #3: The slow junctional escape rhythm in Figure-3 is an additional feature that suggests a recent and/or ongoing OMI (Occlusion-associated Myocardial Infarction) may be present ==> Prompt cath is needed!

A Previous ECG is Found ...

On searching the patient's chart — a previous ECG was found. To facilitate comparison — I've placed both tracings together in Figure-4.

QUESTIONS: 

• What do you learn from seeing this previous ECG? 
• What is the "problem" with this previous ECG?

Figure-4: Comparison of the initial ECG with a previous ECG.

ANSWERS: 

Before addressing the question as to what we learn from Figure-4 — Consider this "problem" with the previous ECG: 

• PEARL #4: All-too-often when I'm sent cases in which a previous ECG is provided for comparison — there is no indication as to what the clinical situation was at the time the prior tracing was recorded.
• For example, in Figure-4 — there are obvious marked abnormalities in the previous tracing. As a result, our approach as to how to interpret this comparison tracing that is now provided to us in Figure-4 may vary greatly depending on whether ECG #2 was recorded:
• During the acute phase of a previous OMI? 
• Immediately after this patient received her stent ~1 year earlier? 
• OR — At a routine follow-up visit after the patient had been pain-free for months?

On further review of this patient's chart — it was learned that this previous ECG was recorded around the time of her stent placement (probably shortly after stent placement in the "culprit" RCA).

• Presumably the deep Q waves in leads II,III,aVF of ECG #2 are the result of the patient's inferior MI — in which some residual ST elevation remains. In addition — there is deep symmetric T wave inversion in the inferior and lateral chest leads of this previous ECG that suggest reperfusion changes that most probably developed following stent placement.
• The overly tall T wave in lead V2 of ECG #2 — is also most probably a reperfusion change from associated posterior OMI.

KEY Point: Despite obvious abnormalities in the previous ECG — We are still able to advance our diagnosis in today's case given the clinical context that today’s patient is now presenting to the ED for acute severe CP beginning just 2 hours prior to the recording of ECG #1. My thoughts regarding Figure-4 were the following:

• The rhythm in today’s initial ECG is no longer sinus. Instead — there is a slow junctional escape rhythm at ~50/minute.
• Although the inferior Q waves are similar to those that were present in the previous ECG — there is now more ST elevation with a hyperacute appearance in each of the inferior leads (in the form of an upsloping, straightened ST segment takeoff).
• Reciprocal ST segment depression in high-lateral leads I, and especially aVL now clearly appears to be hyperacute (with ST segment straightening, prominent terminal T wave positivity, and a gently downsloping ST segment in lead aVL that reflects the mirror-image opposite picture to the ST-T wave in lead III).
• Lateral infarction is suggested by the acute ST elevation in lead V6.
• Finally — the reperfusion changes seen in the chest leads in ECG #2 have virtually resolved (ie, reduced T wave positivity in lead V2 — and resolution of T wave inversion in leads V4,V5).

Bottom Line: 

Given the presentation of new severe CP — comparison of today's initial ECG with the previous tracing suggests there is now acute reocclusion of the RCA — with need for prompt cath!

On reflection of this case — several points deserve emphasis: 

• As helpful as finding the previous tracing was in today's case — the need for prompt cath was already established by: i) The known history of coronary disease; — ii) The presentation of new severe CP just 2 hours before ECG #1 was recorded; — and, iii) The slow junctional escape rhythm in association with limb lead changes in ECG #1 that so clearly look to be hyperacute.
• An elevated Troponin would strengthen the need for prompt cath — but an increased Troponin is not needed to know that prompt cath is indicated (Remember that the initial Troponin may be normal despite acute coronary occlusion — and waiting until Troponin eventually elevated would only incur loss of more myocardium).
• An Echo at the bedside showing a localized inferior wall motion defect would strengthen the need for prompt cath — but this too is not needed to know that prompt cath is indicated (ie, We know this patient had a previous MI — so we would not be able to know if any wall motion abnormality was new or old).
• Although Wellens' Syndrome most commonly presents with ST-T wave abnormalities in the anterior chest leads (from high-grade narrowing of the LAD) — you can see the ST-T wave abnormalities of Wellens Syndrome in any coronary distribution. That said — today's patient presents with new CP — deep Q waves and hyperacute ST elevation — all of which tell us this is not Wellens' Syndrome. 
• Instead — Wellens' Syndrome manifests ST-T wave findings of reperfusion after brief coronary occlusion and before major damage occcurs — with the patient pain-free because the briefly occluded coronary vessel has now spontaneously reopened! 
• (See ECG Blog #350 and ECG Blog #453 — for review of the criteria and findings with Wellens' Syndrome).

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Acknowledgment: My appreciation for the anonymous submission of today's case with these tracings. 

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EXTRA COPY — ECG Blog #532: Wide Tachycardia — EXTRA COPY

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Figure-1: The initial ECG in today's case — obtained from XXXX (To improve visualization — I've digitized the original ECG using PMcardio).

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Figure-2: XXXX

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Acknowledgment: My appreciation to @PrecordialSwirl for submission of today's case with these tracings.

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Arman Bajwa armanbajwa194@gmail.com ME to email Arman whenever this is published !!!

I should say, “My appreciation to — @PrecordialSwirl — for sending me this tracing and this case”

You can keep my real name anonymous but tag my twitter account @PrecordialSwirl, thats where i post all of the same ecgs that I send to you.

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Arman Bajwa — Nurse in Australia

Arman Bajwa armanbajwa194@gmail.com ME to email Arman whenever this is published !!!

I should say, “My appreciation to — @PrecordialSwirl — for sending me this tracing and this case”

You can keep my real name anonymous but tag my twitter account @PrecordialSwirl, thats where i post all of the same ecgs that I send to you.

 

THE CASE:

Hi dr. Grauer — Thanks for replying to my email about the QT interval. This time I have an ECG challenge for you. Pt was early 60s. Developed sudden tachycardia, asymptomattic, no prior history of MI or IHD.

I’d like to know how you would approach this. Then I’ll tell you how we reverted this and what the EP study showed.

Thanks and Kind regards

Arman

MY REPLY:

Hi Arman. Regular WCT (Wide-Complex Tachycardia) at ~170/minute without sinus P waves.

• PINK arrows look like 1:1 VA conduction.
• QRS morphology is perfectly consistent with LBBB conduction (upright R waves in I,aVL,V6 — and very steep initial downslope in the anterior leads).
• So clearly could be a reentry SVT rhythm. If completely stable and presented to an ED — Could try Adenosine as a diagnostic/therapeutic trail (should cardiovert the patient if this is AVNRT or AVRT). For any concerns, or if at any time the patient became unstable — then cardiovert.
• Note: 1:1 VA conduction can occur with both reentry SVTs as well as with VT — so this finding does not help in diagnosis.
• Cannot rule out VT on this single ECG — but morphology suggests SVT more likely.

 

Arman — I’d LOVE to use this case as an ECG Blog! (Readers always love the WCT cases!  — especially when you will be giving me follow-up and EP input! )

• I’d be happy to acknowledge you and/or any of your colleagues (Please tell me the city and country where you are from — OR, the case could be anonymous if you prefer). It may be a little while — as I have other cases to go before this one.
• P.S. — I’m curious — What is your medical specialty? — :)

ARMAN REPLY:

Thanks for your quick response. I’m a new RN working in a cardiology ward in Australia. I just graduated nursing school 3 months ago. Yes I’m happy for you to use the ecg on your blog. You can keep my real name anonymous but tag my twitter account @PrecordialSwirl, thats where i post all of the same ecgs that I send to you.

 

More background- the pt had an SVT ablation 5 years ago but developed palpitations again. Was evaluated outpatient and admitted for an elective ablation. Baseline ECG had no aberrancy. He developed this tachycardia in our ward, a day before his scheduled ablation. Good thing about a telemetry unit is that we could go back in time and see that it initiated with a PAC( I curse myself for not saving that strip). The tachycardia was terminated with 6 of adenosine.

 

EP results- concealed left lateral accessory pathway with no inducible tachycardia. Slow- Fast AVNRT induced and ablated. Rate related LBBB. 

Could this have been orthodromic AVRT? I dont think so, as I said, it initiated with a PAC.

 

However, I still don’t understand why LBB was refractory instead of the RBB, it’s usually the other way around.

 

Thanks and Kind Regards

Arman Bajwa 

EXTRA COPY — ECG Blog #535: A "Fluttering" ECG - EXTRA COPY

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Figure-1: The initial ECG in today's case — obtained from a XXXX (To improve visualization — I've digitized the original ECG using PMcardio).

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Figure-2: XXXXX 

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Acknowledgment: My appreciation to Cardiology Notes (FB ECG site) for allowing me to use this tracing — and to Ahmed Marai (from Anbar, Iraq) for drawing my attention to this case.

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From Ahmed:

Hello Dr. Grauer — I came across this ECG on facebook, which belongs to to a 50-year-old male, hypertensive and diabetic, recorded while he underwent a routine check up.

This is the link to the poster

https://m.facebook.com/story.php?story_fbid=pfbid0wAJTSLDFuYExamcgrFy3RaR1DzcE6xbef7jf77Pdzy8htmBamYTTG5EJNSM2H13zl&id=61563573262961

This is my interpretation:

A 12 lead ECG, unlabelled calibration and speed, but it looks standard.

Ventricular rate: around 62-66 bpm

Rhythm: regular narrow complex rhythm

Axis: within normal range

No obvious P waves, however, there are regular waves between the QRS complexes, which run at around 273bpm, it appears in all the 12 leads and looks much taller in the chest leads compared to the limb leads.

Regarding QRS complex, it is narrow, with very subtle irregularity. In the chest leads, the QRS is dominantly positive (no obvious S waves), and has high voltage in V2-V5.

 

No obvious ST-T changes, and the QT intervals cannot be determined accurately.

Clinical impression: The regular waves seen between the QRS complexes are probably flutter waves, it runs at around 273bpm, and since ventricles beat at around 66bpm, then it is probably AFlu with 4:1 AV conduction. However, these flutter waves are atypically tall in the chest leads.

The high voltage of R waves in chest leads, is suggestive of possible LVH, the history of hypertension may support the possibility of LVH. The S waves are are not obvious in chest leads, but they are possibly present but are cancelled on the paper by the tall flutter waves. 

However, artifact should be suspected and excluded.

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My thoughts: At the beginning I thought this is an obvious atrial flutter with 4:1 av conduction, however, when I noticed the size of flutter waves in the chest leads, I thought this is unusual. 

I saw many people in the comments say, Artifact !! 

If this was an artifact coming from one limb, then one of these leads ( I, II or III ) should be spared. If the artifact is coming from 2 limbs, then it should be chaotic and not regular like this one.

If this was an artifact, then it is probably coming from the patient torso, maybe the patient was dancing while recording the ECG. This may explain why these waves are taller in the chest leads compared to the limb leads, as they are closer to the torso. Excited to hear your ideas on this ECG — Ahmed

MY REPLY:

Hi. I basically AGREE with you!

I’ve attached what I wrote on the FB site.

I also wrote to Cardiology Notes, asking them for follow-up! (They have great cases — but often don’t tells us what happened unless specifically asked!

: ) Ken

P.S. Another clue should be looked for — which is whether the DISTANCE between the closest deflection and the QRS is equal !!! Be SURE to use your calipers when looking for this. Usually (although not always) — IF the ventricular rhythm is regular — then the distance between the closest deflection and the QRS should be THE SAME! If it is not — and if the R-R interval remains constant — then this implies that NONE of the deflections are conducting!

But in this case — there is a very slight-but-real difference in the “PR” interval across lead II ==> IF the R-R interval would stay precisely equal, then if this was Aflutter — it implies complete AV block (which is possible but not common).

So — We wonder if this patient has a tremor, or perhaps something going on in his chest …

CARDIOLOGY NOTES (on Facebook !!! )

Hello Prof Ken. It was ARTIFACT! The patient is diagnosed with drug-induced Parkinsonism !!!!

EXTRA COPY — ECG Blog #534: What is or is not Conducting? — EXTRA COPY

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Figure-1: The initial ECG in today's case — obtained from XXXX (To improve visualization — I've digitized the original ECG using PMcardio).

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Figure-2: XXX

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Figure-3: XXX

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Figure-4: XXX

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Figure-5: XXX

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Figure-6: XXX

Figure-7: XXX

Figure-8: XXX

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