EXTRA COPY — ECG Blog #542 — Why is the Rhythm Irregular? — EXTRA COPY

The ECG in Figure-1 was obtained from a man in his 60s — who is aware of his "irregular heart beat".

Relevant history: 

• The patient is overall healthy — with the exception of some "kidney issues" for which he periodically has "low potassium" and sees a nephrologist.
• The patient notes that his "skipped beats" tend to increase when he is lying down — and generally go away when he stands up.

 

QUESTIONS:

• How to interpret the rhythm in Figure-1?
• What is your differential diagnosis for the irregularity?
• How does the 12-lead ECG help in diagnosing the rhythm?

Figure-1: The initial ECG in today's case. 

ANSWER:

By the Ps, Qs, 3R Approach to systematic rhythm interpretation (See ECG Blog #185) — I note the following:

• The QRS is narrow everywhere. This tells us that the rhythm is supraventricular.
• The Rate is controlled, averaging ~60/minute — but the rhythm is not Regular. Instead, there is a bigeminal rhythm (ie, Every-other-beat occurs early — such that we see a repetitive pattern with groups of 2 beats followed by a short pause). See ECG Blog #232 for more on the types of bigeminal rhythms.
• P waves are present. These P waves precede each of the 9 beats in the long lead II (as per the RED arrows in the long lead II rhythm strip in Figure-2).
• These P waves are "Related" to neighboring QRS complexes — because the PR interval before each QRS complex is constant (as well as being normal = not more than 1 large box in duration).

Figure-2: I've added RED arrows to highlight regularly occurring P waves that precede each QRS with a constant (conducting) PR interval.

Our Differential Diagnosis:

We've arrived at a relatively common situation in that there is a bigeminal rhythm — in which all QRS complexes are preceded by P waves that appear to be conducting because they have a constant PR interval. At this point — my diagnostic considerations were the following:

• Atrial bigeminy (in which every other beat is a PAC). I thought this to be unlikely — because as I look at all 12 leads in the simultaneously-recorded ECG above the long lead rhythm strip — P wave morphology looks to be identical for the early beats ( = beats #1,3,5,7,9) — and for the normal sinus-conducted beats ( = beats #2,4,6,8). Because PACs arise from a different place in the atria — P wave morphology of PACs should differ from the P wave morphology of normal sinus-conducted P waves.
• Atrial trigeminy with blocked PACs (ie, in which every 3rd beat is a non-conducted PAC). This is also unlikely, because as I look at all 12 leads in the ECG above the long lead II — the T waves of beats #1,3,5,7,9 do not manifest any notching or extra peaking that would alert to hidden, non-conducted P waves.
• 2nd-degree AV block of the Mobitz I Type (which is the same thing as AV Wenckebach) is not present because: i) The  PR interval is not increasing within each of the 2-beat groups; — and, ii) The P-P interval is not regular (or at least almost regular) — as it should be if AV block was present.
• 2nd-degree AV block of the Mobitz II Type is not present. This is because the P-P interval is not regular (or at least almost regular) — as it should be if there was some form of AV block.
• Sinus arrhythmia is unlikely to be present here. This is because the rhythm in Figure-2 represents a fixed pattern of group beating, in which the duration of each of the longer, and each of the shorter R-R intervals is remarkably consistent. In contrast — the duration of R-R interval variation is generally longer with sinus arrhythmia, and manifests much more variability than what we see in Figure-2.
• 
  
• SA (SinoAtrial) block . . .

Conclusion: Having ruled out my top 5 diagnostic considerations that I list above — We are left with the last consideration on my list = SA Block!

• The reason I put SA block last on my list — is that true SA block is the least common of the above entities that I encounter. That said — it "fits best" for the characteristics of today's ECG.
• My proposed laddergram in Figure-3 illustrates what appears to be the mechanism of this patient's SA block. 

Figure-3: My proposed laddergram for today's rhythm.

Laddergram Illustration:

I review how to read laddergrams (as well as presenting a primer for how to draw them) — with numerous examples of laddergrams in ECG Blog #188.

• As I illustrate in Blog #188 — it's EASY to read laddergrams that have already been drawn for you. All the laddergram does — is follow the electrical impulse as it records the cardiac rhythm, showing the path of electrical activity as it makes its way through the Atria — then the A-V Node — and finally through the Ventricles.
• In today's case, since the mechanism of the rhythm is SA Block — the problem arises from within the SA Node.

We show this schematically in Figure-3:

• Beginning with beat #2 — We see that only 2 out of every 3 SA nodal impulses ( = the RED circles at the very top of the laddergram) — are able to make it through the SA Node to arrive in the Atria.
• Keeping in mind that time is recorded horizontally — We can see that once an impulse arrives in the atria, that conduction speeds up. We schematically depict this by drawing the lines that pass through the Atrial Tier vertically (representing fast conduction through specialized atrial fibers).
• Conduction of each impulse then slows down as the impulse passes through the AV Nodal Tier (which is why there is slight increase in angulation of the RED lines within the AV Nodal Tier).
• On arrival in the ventricles — conduction again speeds up due to fast conduction through specialized His-Purkinje fibers (less angulation of the RED lines within the Ventricular Tier).

Return for a moment to the SA Nodal Tier at the top of the laddergram: 

• Note the increase in angulation between the 1st and 2nd RED circles in each group — with the 3rd RED circle being blocked — after which the sequence begins again. This is Wenckebach conduction! (ie, There is 3:2 SA block of the Wenckebach Type).
• For more on SA Block — See the ADDENDUM below!

Clinical Correlation in Today's CASE:

Going back to the brief history presented at the beginning of this case — We were told that today's patient has a history of hypokalemia — and that he noticed a tendency for his "skipped beats" to increase when lying down, and to go away when standing up.

• In my experience of having looked for true examples of SA block over decades — this phenomenon is not common in the general population.
• At times I've observed incidental SA block, seemingly without clinical consequence (almost like a normal variant).
• At other times, this rhythm is clearly pathologic — accompanying inferior infarction with 2nd-degree AV block of the Wenckebach (Mobitz I) Type — or — as a component of the arrhythmias seen with SSS (Sick Sinus Syndrome).
• In today's case — I suspect that this patient's periodic hypokalemia was at least contributing to development of his SA block, if not frankly causative.
• Holter monitoring showed this patient's SA block to be without hemodynamic consequence, although persistent through much of the day that the Holter was done. I lack the follow-up to know if the rhythm resolved once serum K+ normalized.
• Otherwise — selected patients with cardiac arrhythmias have been known to observe a change in the frequency of certain rhythm disorders depending on body posture. This effect is highly individualized — with literature on the subject scarce, and the mechanism uncertain. Theories include variation in vagal tone, which tends to increase when resting supine. Other theories involve changes in intrathoracic pressure occurring with changes in body position — and/or increased "stretch" on cardiac tissue seemingly being more likely when supine.
• Bottom Line: It's hard to know what to do with a history that the patient notes of a change in arrhythmia frequency depending on body position — other than to accept that in some selected patients, there is evidence that arrhythmias may increase or decrease depending on body position.

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Acknowledgment: My appreciation to Stewart (from Los Angeles, USA) — for allowing me to use this case and this tracing.

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ADDENDUM:

Figure-4: Essentials of SA Block (Modified from Grauer: ACLS-2013-ePub).

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #312 and ECG Blog #488 — for additional examples of SA block. 
• ECG Blog #147 — Reviews a case showing blocked PACs. 
• ECG Blog #57 — Reviews a case showing atrial bigeminy with blocked PACs.

EXTRA COPY — ECG Blog #543: A 24-Hour Holter was Done- EXTRA COPY

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Figure-1: The initial ECG in today's case.

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Figure-2: XXX

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Figure-3: XXX

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Acknowledgment: My appreciation to ANONYMOUS? OR Passang Jinpa (from Guayaquil, Ecuador) — for allowing me to use this case and this tracing.

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Passang Jinpa — Guayaquil, Ecuador (Cardiologist at a free clinic! ) – 7/31/2026

THE CASE — Passang Jinpa

An 80-year-old woman presented with mild dizziness and fatigue, denying chest pain or dyspnea. Resting12-lead ECG showed marked sinus bradycardia with biphasic T-wave changes in anterior precordial leads, suggestive of a Wellens pattern. Ambulatory heart rate response was preserved. Echocardiography revealed regional wall motion abnormalities in the basal and mid-anteroseptal segments with sinus bradycardia throughout. A 24-hour Holter monitor was ordered.

 

Clinical Timeline: Day 1: Resting 12-lead ECG. Day 2: 24-hour Holter monitoring initiated. Day 3: Patient found deceased while wearing the Holter monitor. Retrospective review of the Holter recording captured the entire electrocardiographic evolution of the acute myocardial infarction, from initial ischemic changes through ST-segment elevation to the terminal arrhythmia.

 

What should I've done at first? Cath lab activation?

On Day-2 when she came to clinic no chest pain, absolutely fine.

 

MY REPLY:

Be sure to carefully review my ECG Blog #350 (https://ecg-interpretation.blogspot.com/2022/12/ecg-blog-350-severe-cp-not-much-on-ecg.html ) that reviews what Wellens' Syndrome truly is. Be sure to also review material in the Addendum (including the 8 minute Audio Pearl). So your patient did not have a true "Wellens' Syndrome" — because there was no history of chest pain that then went away. But it's important to remember the pathophysiology of Wellens' Syndrome (which I review in Blog #350) — as well as the fact that an IDENTICAL ECG may be seen AFTER an infarction. And in older patients — a "silent" MI (ie, an MI but without any chest pain) is the probable explanation for the T wave inversions that we see in your patient's ECG. So my main questions would relate as to WHEN the patient had those symptoms of mild dizziness and fatigue. It is a very fine line as to which older patient who you strongly suspect has had a "silent MI" needs to be hospitalized until you can be comfortable that their condition has stabilized. So — IF this patient's symptoms were in the last day or two — and especially since the heart rate on this ECG is SLOW (about 50/minute) — a period of monitoring in the hospital would seem warranted. Were Troponins done? If so — and if still elevated, that's another clue that this patient's MI was recent — and if this is a fully functioning 80-year old — cardiac cath should probably have been done before sending the patient home. P.S. Again, the history here is very subtle — but serial Troponins and serial ECGs may have provided insight as to WHEN the MI occurred (and the need for cath). Finally — Before I'd want to send this patient home — I would want to see if she is able to walk at a level comparable to doing her everyday activities. Ideally she is monitored when you do that. The point is that many patients don't want to stay in the hospital — but if this 80 yo woman normally is able to walk everywhere — and now she gets fatigued on much less activity — that's one more sign that she has had a recent MI that may not yet have "completed" (such that cath may be indicated before she goes home). TOUGH case. I hope the above is 

helpful ...

 

 

PASSANG Reply:

Dear Guru KEN, Thank you very much for your thoughtful comments and for taking the time to review my case. I really appreciate your insights. This was actually the patient's first medical evaluation. She had never previously seen a physician. I work in a charitable foundation that provides free outpatient cardiology consultations. Although it functions as a private clinic, patients are responsible for any additional investigations or hospital care, and many have significant financial limitations. Clinically, she looked remarkably well. She was an active 80-year-old woman who came with a friend in her 90s. They were both independent, regularly went shopping together, and she denied chest pain or dyspnea. She only mentioned mild fatigue. Because she appeared so functional and stable, I did not initially suspect an acute coronary syndrome. On the first day, I obtained a 12-lead ECG and observed an abnormal T-wave pattern. I ordered routine laboratory tests, but unfortunately I did not obtain troponin levels. Immediate coronary angiography was also not a realistic option because of the patient's financial situation. What makes this case particularly fascinating is what happened afterward. A 24-hour Holter monitor had been placed, and sadly, the patient was found deceased the following day before returning to have it removed. During my retrospective analysis of the Holter recording, I was able to observe the complete electrical evolution—from the initial ischemic T-wave abnormalities, through progressive ST-segment elevation, and ultimately to the terminal rhythm. The transition began at approximately 11:00 PM. To my knowledge, it is uncommon to have continuous Holter documentation of the entire evolution of an untreated myocardial infarction ending in sudden death. I believe this provides a unique opportunity to correlate the initial 12-lead ECG with the continuous ischemic progression. Do you think this case would be suitable for publication as a case report? If so, I would greatly appreciate any suggestions regarding the best way to present it or which aspects should be emphasized.

 

MY REPLY:

Hi. I can totally relate to ALL that you describe. Knowing more of the details — I may have done what you did.

My training is in family medicine. I was faculty in a Family Medicine Residency for 30 years — so we would see ambulatory patients and on occasion we'd get a history similar to what you describe, in which you suspect that an MI occurred days earlier. So the question then arises as to HOW MUCH to do for a "completed MI?" in an older patient who doesn't want to come into the hospital.

I am also familiar with free clinics as you describe (but for which funding is lacking if additional investigations are needed. You deserve CREDIT for providing care to people who otherwise have NO care .... but situations like this one are clearly frustrating!

In retrospect — the only thing I could say is that subtle change in symptoms (ie, development of some new "fatigue" in recent days in an older person with the initial ECG that you show is suggestive that a recent MI may have occurred, and that we are now seeing reperfusion T waves. What to do with this IF the patient otherwise "seems well" is a difficult question and "Ya gotta be there!" because there is NO certain answer.

In my capacity as hospital Attending for 3-4 months each year — I would read all of our service ECGs and I'd see the Holter Monitors. I will NEVER forget reading ECGs one day — and seeing a Holter monitor of a hospitalized patient, when I suddenly saw on the Holter that the rhythm was getting slower and slower — and then stopped. So I ran up to the floor where this patient was — only to find everyone at the bedside treating her cardiac arrest. It was an EERIE feeling seeing that Holter, and then seeing the patient (just like the eerie feeling that I'm sure you have when you saw these tracings!).

The above said — YES, this is rare to catch this — but I'm not sure you have best exposure by writing an article. Instead — I propose that you let me write an ECG Blog Case that I will publish within a couple weeks. I will show the 12 lead ECG that you sent me and ask the reader how they will interpret this?

I will write up the case giving enough basic info to "set the scene" — but I will not give specific details that may identify the patient. And then I will show the sequential tracings you sent me (that I put into a PDF here).

When I was on faculty — I would "collect" code tracings and later went thru them for insight while I was writing my books on ACLS. So these sequential tracings that you sent me show a similar sequence of events as this unfortunate woman evolved her huge extensive LAD occlusion.

These are TOUGH cases. Given age, vague symptoms (!!!) and lack of resources — there is no right or wrong answer — but the fact that you are soul searching events is sign that YOU are truly a good, caring physician doing the best you can given limited resources for the best you can do for your patients. Many clinicians would not give this case a second thought ....

Is it OK with you that I write this case up as an ECG Blog? I would be happy to acknowledge you if you like? — or the case can be anonymous — JUST LET ME KNOW. It will be published as a Blog post on-line, so it can be referenced by a link to my Blog.

Let me know what you prefer. THANK YOU for sharing this very difficult case with me. I believe it IS worthwhile to soul search events and think IF there is anything for you to learn from this OR if in fact you considered everything and from the information you had simply thought this was a completed MI with not much to gain by hospital admission in an older, minimally symptomatic patient. Putting older patients in a hospital is NOT benign, as "things happen" in the hospital ...

Should I acknowledge you as Passang Jinpa from Guayaquil, Ecuador — Dejame saber lo que quieres que hago por este caso — Ken

EXTRA COPY: ECG Blog #541: Obvious MI — What is the Culprit? — EXTRA COPY

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

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

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ADDENDUM:

I have added this Tab on Technical "Misadventures" — to the Menu at the top of every page in this ECG Blog:

— Where to find this LINK in the Top Menu! — 

All-too-often lead reversals, unsuspected artifact, and other "technical misadventures" go unrecognized — with resultant erroneous diagnostic and therapeutic implications. 

• In the hope of facilitating recognition of these cases — I am developing an ongoing listing on this page with LINKS to examples that I’ve published in this ECG Blog, as well as in Dr. Smith’s ECG Blog where I frequently write commentaries.

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O.p. Sanooj ( 10/10/2023 ) — Facebook Messenger

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

— "Obvious MI but WHAT is the Culprit?"

Sure sir, it is a honour for me if you publish this. 

Your earlier advice of giving   IV betablocker and cordarone helped me to kill VT in this case. And also I gave plenty of fluids suspecting RVMI. Thanks from the bottom of my heart sir.

 

THE CASE:

Hi sir, this patient had arrested in cathlab while doing angioplasty. Given CPR for 30 minutes and multiple shocks for VT. Finally after opening RCA, he became stable. Now he is doing well.

 

There is shelf like ST depression in inferior leads, ST elevation in 1, aVL,V6 indicating infero lateral MI. The absence of ST depression in V1 indicates there is RVMI. Am I right sir?

Sir, this is today's ecg. Patient is stable now. There is no occlusion in Lcx. The culprit artery on cath was RCA. I have confirmed it.

MY 1st REPLY (I was initially fooled !!!! — important to tell why!)

Hi. I put the 2 parts together to get a better 12-lead picture. I see sinus rhythm — with as you say MARKED ST elevation in I,aVL and V3-thru-V6. This picture to me is MUCH MORE SUGGESTIVE of acute LCx (Left CircumfleX) occlusion. One of the 2 QRS complexes in lead V2 has slight ST depression (but neither has the usual slight ST elevation) — which to me suggests there is also posterior MI. I am not quite sure why there appears to be slight ST elevation in lead V1 — but everything else on this tracing suggests that the LCx is the "culprit" artery — and the LCx generally does NOT supply the RV ...

 

Are you sure that the "culprit" artery on cath was the RCA? Did this patient have multi-vessel disease ??? — as if he did, then depending on the pattern of collateralization, you may get a different distribution for the ST elevation and depression.

The massive ST depression in leads II,III,aVF is consistent with reciprocal ST depression — which further supports that the main injury is from LCx occlusion.

 

Let me know if you have any follow-up. How is the patient now doing? Any follow-up ECGs? (the distribution of reperfusion T waves might support our theory for what was the "culprit" artery).

MY 2nd REPLY:

NOW I see what is going on !!!! There was LA-LL Lead Reversal on the initial ECG !!!! The usual "clue to this is that the P wave in lead I is larger than in lead II — but that was not at all obvious here, because P waves are almost of similar size. But your post cath ECG shows DEFINITE reperfusion changes in the inferior leads !!! and that would not make any sense if this was an LCx occlusion.

 

I thought lead V1 (as YOU also said) looked funny for LCx occlusion on the original tracing! — and lead II ALSO looked funny, because I would NOT expect reciprocal ST depression — and the AMOUNT of ST elevation in leads I,aVL is more than I've ever seen for LCx occlusion.

BUT — if you make the adjustments that I've made for LA-LL Reversal — then the original ECG fits PERFECTLY with your clinical scenario ( = marked ST elevation in inferior leads with more recip ST dep in aVL than in lead I — and as YOU said, the subtle ST elevation in V1 IS strongly suggestive of acute RV MI! There is also posterior MI which is "masked" because of all the ST elevation in V1,V2 from the RV MI !!!!

And now the post cath ECG makes perfect sense!!!!

I definitely want to use this as an ECG Blog! It may be a month or so until I get to this (because other cases come before) — but do I have your permission to publish this? Please remind me of the city & country from where you are from — as I will acknowledge you and let you know when I publish this. This is a SUPER CASE!

My Blog #396 (https://tinyurl.com/KG-Blog-396 ) is on a lead reversal — but if you scroll down to the bottom of the page — you'll find links to LOTS of lead reversal cases that I've commented on (including a bunch with LA-LL lead reversal) - FASCINATING! — :)

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ECG Blog #375

https://ecg-interpretation.blogspot.com/2023/04/ecg-blog-375-at-least-3-major-findings.html

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The ECG in Figure-1 was obtained from a 50-year old man — who presented to the ED (Emergency Department) with new-onset CP (Chest Pain).

QUESTIONS:

• There are at least 3 principal findings on this ECG — some of which deal with a possible “culprit” artery and/or the location of whatever is going on. How many of these findings can YOU identify?
• 
  
• HINT: Is the rhythm sinus?

Figure-1: The initial ECG in today's case — obtained from a 50-year old man with new chest pain. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the ECG in Figure-1:

As always — I like to start my interpretation of 12-lead ECGs with assessment of the rhythm (as per my systematic approach in ECG Blog-205). Since there is no long lead rhythm strip — I focus my attention on the 3 beats that we see in lead II from the 12-lead ECG shown in Figure-1.

• The QRS complex is narrow — so the rhythm is supraventricular.
• Although we lack a long lead rhythm strip — it appears that the overall rhythm in Figure-1 is Regular — at a Rate between ~80-85/minute (ie, with an R-R interval of between 3-4 large boxes in duration).
• Upright P waves are present in lead II — but there is something unusual about these P waves in lead II. Did you notice this unusual finding that is not typically seen with a normal sinus rhythm?

PEARL #1: Because the overall direction of travel by the electrical impulse with sinus rhythm (as it passes from the SA Node to the AV Node) — is most closely oriented toward the location of lead II in the frontal plane (lead II being located at +60 degrees in the frontal axis plane) — the P wave with normal sinus rhythm should not only be positive in lead II — but also larger in lead II than in lead I (which is oriented at 0 degrees in the frontal plane).

• Note in Figure-1 — that the upright P wave in lead II is clearly smaller than the upright P wave in lead I. While possible that this discrepancy in relative P wave size between leads I and II could be seen with either an ectopic atrial rhythm or certain forms of dextrocardia — this P wave size discrepancy should prompt consideration of the most commonly overlooked form of lead reversal, which is a mix-up of the LA (Left Arm) and LL (Left Leg) electrodes.

What Happens with LA-LL Lead Reversal?

My favorite on-line “Quick GO-TO” reference for the most common types of lead misplacement comes from LITFL ( = Life-In-The-Fast-Lane). I have used the superb web page they post in their web site on this subject for years. It’s EASY to find — Simply put in, “LITFL Lead Reversal” in the Search bar — and the link comes up instantly.

• This LITFL web page describes the 7 most common lead reversals. There are other possibilities (ie, in which there may be misplacement of multiple leads) — but these are less common and more difficult to predict.
• 
  
• By far (!) — the most common lead reversal is mix-up of the LA (Left Arm) and RA (Right Arm) electrodes. This lead reversal is usually EASY to spot — because it typically produces global negativity of the P wave, QRS and T wave in lead I — which is something that is virtually never normally seen (See ECG Blog #264 — for an example of LA-RA lead reversal).
• 
  
• In contrast — it is EASY to overlook LA-LL reversal — because the ECG picture seen with this type of lead reversal does not immediately stand out as physiologically “off”. For clarity — I’ve reproduced with slight modification the illustration from LITFL on LA-LL reversal in Figure-2.

Figure-2: LA-LL Lead Reversal (adapted from LITFL).

What Should the Initial ECG in Today's Case Look Like?

For clarity — I've taken the limb leads from the initial ECG in today's case ( = ECG #1) — and inverted lead III — switched leads I and II — and switched leads aVL and aVF. The result is ECG #1a — which is seen in the righthand portion of Figure-3. 

• Note that the chest leads in ECG #1a of Figure-3 — are unchanged from what they were in Figure-1.

QUESTIONS:

Looking at ECG #1a in Figure-3:

• Is the P wave in lead II of ECG #1a now larger than the P wave in lead I (as it should be with a normal sinus rhythm)?
• 
  
• Now that we've established that the 1st KEY finding in today's case is that there was LA-LL Lead Reversal — How would YOU interpret ECG #1a, which shows what today's 12-lead ECG would look like IF lead placement was correct?

MY Interpretation of ECG #1a:

Having accounted for what today's initial tracing would have looked like had lead placement been correct — I see the following in ECG #1a:

• The rhythm is sinus at ~80-85/minute.
• There is dramatic ST elevation in each of the inferior leads. A Q wave is forming in lead II.
• There is equally dramatic reciprocal ST depression in lead aVL (which manifests the mirror-image opposite ST-T wave picture as seen in lead III).
• Significant reciprocal ST depression is also seen in the other high-lateral lead ( = lead I).
• 
  
• In the chest leads — there is significant ST elevation, with a straightened ST segment takeoff in lead V1.
• There is abrupt transition to a surprisingly tall R wave (of ~10 mm) already by lead V2. There is significant ST depression with a positive "Mirror" Test for acute posterior infarction in lead V2. Chest lead ST depression is limited to lead V2.
• There is marked overlap of QRS complexes in virtually all chest leads. The deep anterior S waves and tall lateral chest lead R waves suggest significant LVH.

Putting It All Together: 

After correcting for LA-LL lead reversal — ECG #1a shows sinus rhythm — LVH — and an acute infero-postero STEMI with acute RV involvement.

• PEARL #2: The "culprit" artery in today's case — is almost certain to be the proximal RCA (Right Coronary Artery). As discussed in ECG Blog #141 — ECG features in Figure-3 that strongly support the likelihood of the RCA as the "culprit artery" are: i) ST elevation in lead III>II; ii) Marked reciprocal ST depression in lead aVL; iii) Relatively less (or no) lateral ST elevation, with the amount of ST elevation in lead III > V6; and, iv) Evidence of acute RV involvement. 

PEARL #3: In the absence of an anterior STEMI — acute inferior MI is the result of either acute RCA or LCx (Left Circumflex) coronary occlusion. The LCx does not supply the right ventricle. Therefore, if there is ECG evidence suggesting acute RV involvement in association with inferior STEMI — this is virtually diagnostic of the proximal RCA being the culprit artery. 

• ST elevation in right-sided leads (especially in lead V4R) is clearly the best indicator of acute RV MI. That said — lead V1 is a right-sided lead, and on occasion it may provide insight as to whether or not there is likely to be significant associated RV infarction. 
• Normally the ST segment in lead V1 is flat or slightly depressed. With acute inferior STEMI — ST segments in leads V1, V2 and V3 often show ST depression due to accompanying posterior infarction and/or reciprocal changess due to the inferior STEMI. Typically, such ST depression is maximal in lead V2 — but it should also be present in V1. If ever there is ST segment coving (especially if accompanied by some ST elevation) in lead V1 — there is almost certainly acute RV involvement. This is precisely what we see in lead V1 of ECG #1a.

Figure-3: Comparison of the limb leads from the initial tracing in today's case ( = ECG #1) — with what the initial 12-lead ECG would have looked like ( = ECG #1a) after correction to account for LA-LL Lead Reversal. (To improve visualization — I've digitized the original ECG using PMcardio).

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Acknowledgment: My appreciation to Adem Ahmed (from Nouakchott, Mauritania) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
• ECG Blog #185 — Review of the Ps, Qs, 3R Approach for systematic rhythm interpretation.
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• ECG Blog #190 — When to suspect acute RV Infarction?
• ECG Blog #141 — On acute RCA Occlusion (with RV MI).
• ECG Blog #80 — More on the "culprit" artery.
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• ECG Blog #193 — illustrates use of the Mirror Test to facilitate recognition of acute Posterior MI. This blog post reviews the basics for predicting the "Culprit" Artery (as well as reviewing why the term "STEMI" — should replaced by "OMI" = Occlusion-based MI).
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• ECG Blog #285 — and ECG Blog #246 — and ECG Blog #80 — for examples of acute posterior MI (with use of the Mirror Test to facilitate diagnosis). 
• ECG Blog #317 — reviews use (or not) of Posterior Leads.
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• ECG Blog #184 — and ECG Blog #167 — review the "magical" mirror-image opposite relationship between lead III and lead aVL that helps to confirm acute OMI.
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• ECG Blog #264 — For review of another limb lead reversal (ie, LA-RA lead reversal in a patient with an acute MI).

OTHER Examples of Lead Reversal (from Dr. Smith's ECG Blog):

Technical errors featuring a variety of lead reversal placements remain a surprisingly common “mishap” of everyday practice. As a result — it's important to familiarize ourselves with how best to recognize the various forms of these "misadventures". For review — Check Out My Comment — at the bottom of the page in the following posts on Dr. Smith's ECG Blog:

• The June 4, 2018 post (LA-LL reversal).
• The July 29, 2018 post (LA-RA reversal).
• The November 4, 2018 post (Leads V1,V2 misplacement).
• The February 11, 2020 post (LA-RA reversal).
• The March 18, 2020 post (LA-RA reversal).
• The August 28, 2020 post (LA-LL reversal).
• The November 19, 2020 post (LA-LL reversal).
• The November 27, 2021 post (LA-RA reversal).
• The April 17, 2022 post (Leads V1,V2 misplacement).
• The May 24, 2022 post (LA-LL reversal).
• The May 26, 2022 post (LA-LL reversal).
• The August 17, 2022 post (LA-RA reversal).

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