Wednesday, May 6, 2026

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 in 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 stable at this heart rate?); — andii) 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 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); — andiiiLead 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 witongoing severe CP (Chest Painthat 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!


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; — andiiiThe 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 presented 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 (See ECG Blog #350 and ECG Blog #453 — for review of the criteria for 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 #531: 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 #532: 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
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.
——————————————————————-

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 !!!!






Saturday, May 2, 2026

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



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Figure-13: XXX



Figure-14: XXX



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Tuesday, April 28, 2026

EXTRA COPY — ECG Blog #533: A Surprise Diagnosis — EXTRA COPY

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






https://www.powerfulmedical.com/
https://ecg-interpretation.blogspot.com/2024/08/ecg-blog-443-40s-man-with-cp-and-dyspnea.html


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Figure-2: "My Take" on defining the ST segment baseline (from Grauer K: ECG Pocket Brain-2014 ePub).

 

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Figure-3: I've labeled today's initial ECG.




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Figure-4: ECG Findings associated with acute PE (updated since ECG Blog #443).




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Acknowledgment: My appreciation to Mohammed Elsisi (from Cairo, Egypt) for the case and these tracings.

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=======================

Related ECG Blog Posts to Today’s Case: 

  • ECG Blog #443 and ECG Blog #496 — Review challenging cases on the ECG diagnosis of acute PE.
  • ECG Blog #313 and ECG Blog #435 — Review more cases on the ECG diagnosis of acute PE.
  • ECG Blog #233 — Reviews a case of Acute PE (with discussion of ECG criteria for this diagnosis).
  • ECG Blog #119 — Reviews a case of Acute PE (and ECG criteria for this diagnosis).
  • My Comment at the bottom of the page in the June 17, 2024 post in Dr. Smith's ECG Blog (regarding a case similar to today's ECG Blog).

  • ECG Blog #234 — Reviews ECG criteria for the diagnosis of RVH and RV "Strain".
  • ECG Blog #77 — Another review of ECG criteria for the diagnosis of RVH and RV “Strain”





Mohammed Elsisi <mohammedelsisi18@gmail.com> 4/24/2026
E-Mail from Mohammed 


THE CASE:

This tracing was obtained from a 45 y male pt who presented to the ER with burning chest pain on off for about 1 week with also reproduction of pain with minimal exertion along with dyspnea.

Pt was vitally stable 

I rapidly i terpreted this as sinus tachy with old inferior infarct & may be lad omi based on amputated r in rt precordial leads along with straightening of st segment with rounded peaked ample t waves. 

What's ur take? 

Thank in advance kenneth. 


MY REPLY:

Hi. This is a very worrisome tracing!

  • There is sinus tachycardia (which of itself is a worrisome sign — since sinus tach is uncommon with acute MI unless “something else” [ie, heart failure, shock] is going on … ).
  • As you say — there are inferior Q waves in a “qRS” pattern, which in the inferior leads almost always means an Inf. MI at some point in time.
  • At the least — there is DSI ( = Diffuse Subendocardial Ischemia) — as indicated by the ST elevation in aVR, with ST depression in the other 5 limb leads.

I suspect there is a Precordial “Swirl” pattern — with clearly abnormal ST elevation & T inversion in V1 — and ST segment straightening with ST elevation in leads V2,V3 — and what looks to be some J-point depression in V6. “Swirl” typically is from acute or recent proximal LAD occlusion. The loss of R wave from V2-to-V3 suggests anterior infarction.


The difficult question is what is new vs old — and if new (as I suspect) — how new given the 1 week history of intermittent CP.

  • Any prior history of heart disease in this patient?
  • Any prior ECG available?
  • The patient needs prompt cath — with my suspicion of an LAD “culprit” artery.

Please give me follow-up. If you can find out what happened — I would love to use this case for an ECG Blog. LET ME KNOW.  — Ken

 

= = = = = = = =

Mohammed REPLY:

Thanks ken, as u mentioned pt was admitted in the ccu as ACS. Bedside echo done showed a dilayed rv with d shaped septum thrn CTPA show bilateral pe. 

Back to the ecg one may note that prominent s in lead i ste in rt precordials & deeps in v4 to v6 along woth sinus tachy all may be ecplained with the pe as a final Dx. 

Finally echo was the only clue to us to suspect pe instead of ACS. Pt also now is stable on iv enoxaparin. We do simple work up for hidden malignancy pelviabdominal US ct chest PSA. Thanks in advance.

MY REPLY:

Hello Mohammed. Bedside Echo is invaluable !!! Once you are trained in it — you can do within minutes and you learn so much. If the etiology is an acute MI — then finding a localized wall motion abnormality is strongly supportive of that (with the 1 caveat being that when you have DSI — if there is global dysfunction, then you might not recognize the wall motion abnormality, unless overall LV function was greatly depressed in symmetric fashion).

 

In the “retrospectscope” — in addition to the sinus tachycardia (which as I said, is unusual with acute MI unless there is “something else” going on) — there are S waves everywhere !!! (in virtually all 12 leads! ) — and that can be a sign of acute right heart strain.

  • That said — I did not suspect acute PE given the history of CP ….

 

So — I always like to go back in cases like this and “soul-search” and try to figure out what clues were missed. What did WE miss?

  • ST elevation in lead V1 with T wave inversion in this lead can be a sign of acute RV “strain”!
  • I fully admit that I still did not suspect acute PE, because the SHAPE of the ST depression in this tracing looks different that that usually seen with acute PE (ie, no T wave inversion) — and because of those inferior Q waves — and because of the ST straightening and ST elevation in V2,V3

 

KEY POINT — You did mention “dyspnea” — but you said “vitally stable”. I assumed “vitally stable" meant that the patient’s RR ( Respiratory Rate) was normal.

  • In my experience — the most commonly overlooked vital sign is the respiratory rate. Much of the time — the clinician at the bedside does not take the time to COUNT the respiratory rate. Nurses also (in my experience) of do not count the respiratory rate, but instead put down 12 or 15/minute if the patient “seems OK”.
  • This clearly is something that “Ya gotta be there — at the bedside” — but unless the clinician spends a moment to LOOK at the patient — it is all-too-easy to miss a patient taking rapid but small breaths unless you actually COUNT the breaths per minute — and if the patient was breathing 25-30/minute at rest — in addition to sinus tach — diffuse S waves — and that abnormal isolated ST elevation in lead V1 — acute RV failure could be all too easy to miss ….
  • In retrospect — right-sided leads would probable show right-sided ST elevation.
  • FINALLY — Did this patient ever have an ECG before? Comparison with a prior tracing may have been helpful. That said —it could be that ALL of the ECG findings that we see here are acute as a result of acute PE ….

     

    Bottom Line — Acute PE may present with a “Pseudo-infarction” pattern! (although usually there is more ST elevation in inferior or anterior leads in such cases … )

    • Having said all of the above — I still “fell into the trap” of thinking this ECG looked more like coronary disease than acute MI …

     

    Any more info you can provide would be helpful = What happened? How is the patient doing?

     

    MAY I WRITE this case up for an ECG Blog?

    • If so — Would you like me to acknowledge you OR do you prefer the case is anonymous?
    • If you’d like me to acknowledge you — please confirm if you’d like your name written as Mohammed Elsisi — and tell me the city and country from where you are from?

     

    THANKS! — Ken


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ECG Blog #443
https://ecg-interpretation.blogspot.com/2024/08/ecg-blog-443-40s-man-with-cp-and-dyspnea.html
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The ECG in Figure-1 was obtained from a man in his 40s — who presented to the ED (Emergency Department) because of CP (Chest Pain) and shortness of breath.


QUESTIONS:
  • In view of the above history — How would YOU interpret the ECG in Figure-1?
  • Based on the history and the patient's initial ECG — the cath lab was activated. Do you agree?

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


MY Thoughts on this CASE:
Not being there — I am unaware of physical exam parameters (blood pressure, respiratory rate; oxygen saturation; heart and lung auscultation, etc.). What we can comment on, given the brief history of new CP and dyspnea — is the initial ECG shown in Figure-1I see the following:
  • There is sinus tachycardia (upright P wave with fixed PR interval in lead II) — at the rapid rate of ~130/minute.
  • Regarding intervals — the PR interval is normal — the QRS is of normal duration. Given the rapid rate — it is hard to say much about the QTc.
  • There is RAD (Right Axis Deviation) — in that that QRS is slightly more negative than positive in lead I ( = estimated frontal plane axis about +100 degrees).

Regarding chamber enlargement — LVH is not present. Although frank criteria for RVH (Right Ventricular Hypertrophy) are not present — there are a number of ECG findings consistent (if not suggestive) of acute RV "Strain" (See Figure-2)
  • PEARL #1: Before going further — We need to consider the possibility of acute PE (Pulmonary Embolism)! Acute PE remains one of the most commonly overlooked diagnoses. As per links that I provide below — IF the diagnosis of acute PE is not thought of, this entity will be missed! (See ECG Blog #435 — ECG Blog #313 — as well as My Comment at the bottom of the page in the June 17, 2024 post in Dr. Smith's ECG Blog).

I review the ECG diagnosis of acute RV "strain" and acute PE in the ADDENDUM below (See Figures-7-8-9). For now — Let's continue with ECG signs consistent with and suggestive of acute RV "Strain".
  • Sinus Tachycardia and RAD — as already noted above.
  • PEARL #2: In the absence of associated heart failure (cardiogenic shock) — sinus tachycardia is not a common finding in acute MI. As a result — the finding of sinus tachycardia in today's patient, who presents with both CP and shortness of breath (especially to as rapid a heart rate as the ~130/minute seen here) — should immediately prompt consideration of something other than acute coronary occlusion.

  • Although criteria for RAA (Right Atrial Abnormalityare not strictly satisfied (P wave amplitude in lead II does not attain 2.5 mm in amplitude) — the P wave in lead II is more peaked and pointed than it usually is (within the RED oval in Figure-2). In the context of a suggestive clinical history and other ECG signs of acute RV "strain" — I interpret more-than-expected inferior lead P wave peaking as suggestive of RAA, therefore another supportive (albeit subtle) indication of RV "strain" (See ECG Blog #75 — for more regarding ECG criteria for RAA).

  • S1Q3T3 — Whereas the diagnostic value of this pattern is limited when seen as an isolated finding — a definite S1Q3T3 pattern (as seen in Figure-2) — is very helpful in today's case, given association with other ECG evidence pointing to the possibility of acute PE. 

  • PEARL #3: ST-T wave findings of acute RV "Strain" — are most often seen in the form of anterior T wave inversion (and/or anterior ST depression). The other ECG area to look for RV "strain" — is in the inferior leads, though it is less common in my experience to only see RV "strain" inferiorly without also seeing ST-T wave changes anteriorly.
  • As a result — I admittedly, was initially deterred from the diagnosis of acute PE because of the lack of anterior T wave inversion in ECG #1. That said — ST-T wave changes of acute RV "strain" are present in each of the inferior leads (BLUE arrows in leads II,III,aVF in Figure-2).

  • PEARL #4: Instead of anterior lead T wave inversion — there is some ST elevation in leads V1 and V2, with ST segment straightening in lead V3. On occasion — such anterior lead ST elevation (instead of T wave inversion) can be seen with acute PE (Zhan et al — Ann Noninvasive Electrocardiol 19(6):543-551, 2014 — and — Omar HR — Eur Heart J: Acute Cardiovascu Care (5(8): 579-586, 2016)
  • Right-sided leads such as leads IIIaVR and V1 — face the anterior region of the RV. If the RV is enlarged — then leads V2 and V3 may also face the anterior region of the RV — and — if there is severe transmural ichemia of the RV, any of these leads may show ST elevation (as is seen in leads aVR and V1,V2 in Figure-2).

PEARL #5:
 The KEY for being able to suspect acute PE from the ECG — is when you see a constellation of ECG findings potentially consistent with this diagnosis (as listed below in the ADDENDUM in Figure-7) — in a patient with a suggestive history
  • Today’s patient presented to the ED not only with chest pain — but also with shortness of breath, therefore with a history potentially consistent with the diagnosis. 
  • Easily attainable bedside findings that further support the diagnosis of acute PE include a low oxygen saturation — and — an increased respiratory rate. To emphasize — Count the respiratory rate yourself! (Reading the respiratory rate off of nursing notes is not necessarily accurate in my experience — so spending 15-20 seconds simply looking at the patient breathing and counting breaths is well worth this short amount of your time).

  • ECG Signs (in addition to those already mentioned above) — that are consistent with acute PE in today’s tracing (as per the Table in Figure-7) include: i) Poor R wave progression, with persistence of S waves through to lead V6; andii) The rSr' morphology seen in lead V1, which in association with the narrow terminal s waves in lateral leads I and V6 — is consistent with a IRBBB proxy (See labeled Figure-2 below).

Figure-2: I've labeled the initial ECG in today's case.


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QUESTION: 
Although today’s initial ECG is potentially consistent with acute PE — I would not be 100% convinced of this diagnosis from the tracing shown in Figure-2 alone.
  • What could be done at the bedside within no more than a few minutes to verify the diagnosis of acute PE?




ANSWER:
  • A POC (Point-Of-Care) ECHO — will sometimes be diagnostic of acute PE. When it is — this may greatly expedite clinical decision-making for anticoagulation and/or thrombolysis.
  • The sensitivity of POC Echo is not perfect. That said — the specificity of Echo for acute PE can be excellent IF certain echocardiographic findings are present. This is especially true for larger, more hemodynamically significant PEs — with prognostic insight provided depending on the degree of impairment of RV function (On and Park — Korean J Intern Med: 38(4);456-470, 2023 and Hritani et al — Cleveland Clin J Med 85(110: 826-828, 2018).

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The ECHO on Today's Patient:
In Figure-3 — I've labeled the 4-chamber view from the Echo on today's patient. In Figure-4 — I've included the video recording of this view. What do you think?

Figure-3: Still picture of the Echo 4-chamber view.



Figure-4: Video recording of this 4-chamber view. I include a slow-motion section to facilitate recognition of the diagnostic Echo sign described below.


Figures-3 and -4 on Today's Echo:
For orientation — the 4 chambers are shown in Figure-3:
  • The RV (Right Ventricle) is clearly dilated, and appears to be even larger than the LV. As a result of RV overload — the IVS (InterVentricular Septum) is shifted toward the left side of the heart. In a patient with a suggestive history and ECG findings consistent with acute PE — seeing this degree of RV dilation on Echo strong favors acute PE as the diagnosis. That said — seeing RV dilation on Echo does not distinguish between acute vs chronic causes of RV "strain".

  • PEARL #6: In contrast to the finding of RV dilation (that could be a longstanding condition) — the McConnell Sign is a dynamic echocardiographic finding that is specific for conditions causing acute RV "strain", such as acute PE

  • McConnell Sign is said to be present when 2 echocardiographic findings are seen: i) There is RV free wall akinesis (seen as per the YELLOW arrow in Figure-3 — as an outward movement of the RV free wall as a result of increased pressure in the dilated RV chamber)andii) The RV apex manifests hypercontractility, as a result of being "tethered" to the LV (RED arrow moving inward). This sign is positive in the video recording shown in Figure-4 — in which the RV apex has been described as "a trampoline bouncing up and down while the rest of the RV remains still."

  • References on Echo for PE Diagnosis: Oh and Park - Korean J Intern Med 38(4):456-470, 2023 — and — Hritani et al - Cleveland Clin J Med 85(11):826-828, 2018 — and — IF you want an excellent 5-minute video review on recognition of the McConnell Sign on Echo — WATCH_this_VIDEO by Dr. Christopher Voscopoulos.

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Diagnostic CTPA on Today's Patient:
Final confirmation of acute PE in today's case was obtained by CTPA = Pulmonary Angiography in Figure-5)

Figure-5: CTPA view in today's case — showing large clot burden in the right and left main pulmonary arteries.


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CASE Follow-Up:
The "good news" in today's case — is that the patient received thrombolytics, and ultimately did well. That said — the diagnosis of acute PE was delayed for a number of hours, because providers were initially more concerned about an acute MI. As a result — diagnostic Echo was not performed until after cardiac cath was found to be normal.
  • PEARL #7: Echo at the bedside is a fast test that takes only minutes! In today's case — the Echo could have been done while waiting for cath facilties to get ready. Had this been done — the dramatic RV dilation and positive McConnell Sign seen in Figures-3 and -4 — would have allowed immediate confirmation of acute PE that could have avoided any need for cardiac cath, thereby expediting initiation of thrombolytic therapy.

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Repeat ECG After Thrombolytic Therapy:
I found it of interest to compare the follow-up ECG obtained after successful thrombolytic therapy (Figure-6).
  • Sinus tachycardia has resolved.
  • Right axis deviation in ECG #2 is much less (predominant positivity of the R wave in lead I has returned).
  • RV "strain" is no longer evident (resolution of ST depression in the inferior leads).
  • Right-sided ST elevation that had been present in leads aVR, V1,V2 of ECG #1 — is no longer seen in the repeat tracing.
  • S waves no longer persist through to lead V6.

Figure-6: Comparison between the initial ECG in today's case — with the repeat ECG obtained following thrombolytic therapy.



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Acknowledgment: My appreciation to Magnus Nossen (from Fredrikstad, Norway) for the case and these tracings.

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Related ECG Blog Posts to Today’s Case: 

  • ECG Blog #313 and ECG Blog #435 — Review cases on the ECG diagnosis of acute PE.
  • ECG Blog #233 — Reviews a case of Acute PE (with discussion of ECG criteria for this diagnosis).
  • ECG Blog #119 — Reviews a case of Acute PE (and ECG criteria for this diagnosis).
  • My Comment at the bottom of the page in the June 17, 2024 post in Dr. Smith's ECG Blog (regarding a case similar to today's ECG Blog).

  • ECG Blog #234 — Reviews ECG criteria for the diagnosis of RVH and RV "Strain".
  • ECG Blog #77 — Another review of ECG criteria for the diagnosis of RVH and RV “Strain”

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ADDENDUM #(8/16/2024): 
I've included below some review material regarding the ECG diagnosis of acute PE (Pulmonary Embolus) and RV "strain".


Figure-7: ECG Findings associated with acute PE (from ECG Blog #435).


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PEARL #8: The "Note" under the S1Q3T3 finding in Figure-7 — refers to data from Kosuge et al (Am J Cardiol 99(6): 817-821, 2007 — and the March 4, 2023 post in Dr. Smith's ECG Blog) — that state that when there is T wave inversion in the chest leads, if T waves are also inverted in leads III and V1 — then acute PE is far more likely than acute coronary disease (See the Addendum ECG in Figure-10 below).
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Figure-8: Summary of KEY findings in the ECG diagnosis of acute PE (from my ECG-2014-ePub).




Figure-9: Summary (Continued) of KEY findings in the ECG diagnosis of acute PE.

 




ADDENDUM #(8/17/2024): 
My thanks to Konstantin Tikhonov (from Moscow, Russia) — who sent me the following illustrative ECG and case the very next day after I posted this ECG Blog #443.
  • The patient whose ECG is shown in Figure-10 — had progressively increasing dyspnea over a 10 day period.
  • Considering the ECG findings shown above in Figure-7 (with attention to PEARL #8) — How many ECG findings of acute PE can you identify?


Figure-10: Addendum ECG (My thanks to Konstantin Tikhonov for sending me this case)


ANSWER:
The ECG in Figure-10 shows the following findings in favor of acute PE:
  • Sinus tachycardia.
  • S1Q3T3.
  • Persistent precordial S waves (through to lead V6).
  • Acute RV "strain" (here in the form of deep, symmetric chest lead T wave inversion that is maximal in leads V2,V3,V4 — and as per PEARL #8, shows T wave inversion in lead V1 and lead III, as well as in lead aVF).

Follow-Up: Pulmonary CT scan confirmed an acute submassive PE.