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-1. I 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 Abnormality) are 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 III, aVR 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; and, ii) 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. 

  • A 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); and, ii) 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”. 

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

ADDENDUM #1 (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 #2 (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.
















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