ECG Blog #553 — What happened?

The ECG in Figure-1 was obtained from an older woman — who presented with a 2-hour history of new-onset severe CP (Chest Pain). Her CP then lessened by the time she was seen.

QUESTIONS:

• Obviously this is a STEMI. That said — What ELSE would you say about this tracing?
• What is the probable “culprit” artery?

Figure-1: The initial ECG in today's case — obtained from an older woman with new-onset severe CP. (To improve visualization — I've digitized the original ECG using PMcardio).

My Thoughts on the ECG in Figure-1 …

That this patient is in the midst of an extensive acutely evolving STEMI — is obvious from across the room. But there are a number of additional findings that should be immediately recognized for optimal management.

• The rhythm is sinus tachycardia at a rate of ~130/minute, with 1 PVC (Premature Ventricular Contraction) best seen toward the end of the long lead II rhythm strip (See Figure-2 below).
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• PEARL #1: Most of the time with uncomplicated acute infarction — the patient will not manifest sinus tachycardia. As a result — the finding of any degree of sinus tachycardia should immediately suggest that something else is going on.
• That “something else” could be hypotension (from cardiogenic — or any other form of shock) — or it could be in association with a normal BP and some other acute entity (ie, acute pulmonary disease, acid-base or electrolyte abnormality, anemia, acute GI bleed, etc.).
• Given how extensive the ST elevation in Figure-1 is — and given how fast this sinus tachycardia is ( = ~130/minute! ) — the risk of lethality in this patient with extensive acute ischemia is huge unless prompt cath with PCI is urgently undertaken.

Marked ST-T wave deviation is seen in 11/12 leads in Figure-1:

• RED arrows highlight dramatic ST elevation.
• BLUE arrows highlight reciprocal ST depression
• Lead aVR shows marked ST depression.
• In the midst of all this ST-T wave deviation — Lead V1 is remarkable for its absence of ST elevation or depression.

QUESTIONS: 

• Given that 2 of the 3 inferior leads show reciprocal ST depression (BLUE arrows in leads II and III) — WHY does lead II (which is the 3rd inferior lead) show ST elevation instead of ST depression? 
• Why is there marked ST depression in lead aVR? As discussed in ECG Blog #400 — Usually with DSI (Diffuse Subendocardial Ischemia) there is ST elevation in lead aVR instead of ST depression.
• And why is there practically no ST-T wave deviation in lead V1?

Figure-2: I've labeled KEY findings from Figure-1.

PEARL #2: While we clearly do not need answers to the above questions to recognize the need for prompt cath — appreciation of the answers to these questions is insightful for identifying the likely “culprit” artery. 

• ANSWER: I suspect the reason for some of the unexpected findings in today's initial ECG — is that this patient is presenting with acute occlusion of the LMain (Left Main) coronary artery. 

Acute LMain Coronary Occlusion:

Most patients with acute LMain occlusion do not survive to make it to the hospital. Instead — terminal VFib is the usual result, occurring before medical providers with a defibrillator can get to the patient. For this reason — we rarely see what the ECG looks like when there is acute LMain occlusion (which is why collecting data on these patients is so difficult).

• Dr. Stephen Smith's ECG Blog provides us with rare insight into the ECG findings that may be encountered with acute LMain occlusion. I refer you to the December 18 2025 post in his blog — in which I've updated Dr. Smith's collection of ECGs obtained from patients presenting with documented acute LMain occlusion. As shown below in Figure-3 — this collection now contains 9 patients.

PEARL #3: When a patient with acute LMain occlusion survives long enough for medical providers to record an ECG — You might see anything! 

• The reason why we might see anything is simply because we have multiple different vectors of ST-T wave deviation from varied contributions of all major coronary arteries. Some give ST elevation vectors — others give reciprocal ST depression. 
• In any given patient — it is impossible to predict which of these multiple vectors will dominate with ST elevation not cancelled out by opposing ST depression.
• For example, in Figure-2 — The probable reason why there is ST elevation rather than reciprocal ST depression in lead II — is that at the time that this ECG was recorded, the vector of ST elevation from acute LCx occlusion predominated over the inferior lead reciprocal ST depression vector expected with acute proximal LAD occlusion.
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• Bottom Line: It is rare that you will encounter a patient with acute LMain occlusion. It is virtually impossible to predict what the ECG will look like in such patients. Lead aVR does not provide the answer (as shown in Figure-3 — Lead aVR may show anything!). But at least the findings in Figure-3 give us an idea of the possibilities.
• See ECG Blog #374 — for another case in which acute LMain occlusion is suspected, but could not be proven.

Figure-3: Reasons for the varied ECG presentation of acute LMain occlusion — with this summary synthesized from My Comment in the December 18, 2025 post of Dr. Smith's ECG Blog.

The CASE Continues:

By the time today's patient arrived at the hospital — her chest pain had significantly decreased, and her condition was stabilizing.

• A repeat ECG was obtained (seen in Figure-4).

QUESTION: How would you interpret the repeat ECG? 

Figure-4: Comparison of the repeat ECG with the initial tracing.

The repeat ECG:

The "good news" on seeing the repeat ECG in Figure-4 — is that the patient's CP was less and her condition appeared to be stabilizing.

• The rhythm is still sinus tachycardia, albeit at a slightly slower rate (down from 130 — to 120/minute in ECG #2).

As to ECG #2 — There is less ST elevation compared to the initial ECG. That said — there has been a change in the distribution of acute ST-T wave changes:

• Lead V1 now shows ST segment straightening and elevation.
• Although there is decidedly less ST elevation in the chest leads — there is now ST segment straightening in lead V2, still with ST elevation and a hyperacute appearance to the ST-T waves in leads V2,V3,V4. 
• Surprisingly, there is now a hint of ST depression in lead V6. 

Impression: The chest leads in ECG #2 now strongly suggest the pattern of precordial Swirl consistent with acute proximal LAD occlusion (See ECG Blog #380 — for review of Precordial Swirl). To emphasize — that the pattern of "Swirl" was not present in ECG #1 in which there was no ST elevation in lead V1, and no hint of ST depression in lead V6.

• Regarding the limb leads in ECG #2 — there is no longer the marked ST elevation in leads I,II,aVL. Instead — We now see reciprocal ST depression in all 3 inferior leads (leads II,III,aVF).
• The marked ST depression that had been seen in lead aVR is no longer present.

PEARL #4: I have been repeatedly amazed at how much easier it is to appreciate subtle-but-important differences between serial tracings when you put both ECGs together, and assess the 2 tracings by lead-to-lead comparison. Until I did this — the only thing I appreciated was that ECG #2 looked "better" than ECG #1. 

• I suspect that today's patient presented with acute LMain occlusion. The subtle changes described above that we see in Figure-4 can best be explained by some amount of spontaneous reperfusion of the LMain coronary artery that must have allowed some perfusion of the LCx (which is why the dramatic ST elevation that we saw in leads I,aVL; V4,V5,V6 in ECG #1 has almost completely resolved).
• As a result of this restoration of flow in the LCx — the ST-T wave changes of acute proximal LAD occlusion are no longer attenuated by blocked flow in the LCx (which is why we now see the unopposed Precordial Swirl pattern in the chest leads of ECG #2). It is also why we now see reciprocal ST depression in all 3 inferior leads, with slight ST elevation in lead aVL and less ST depression in lead aVR.

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Today's CASE Concludes ...

Given this patient's improving clinical condition — the decision was made not to perform emergent cardiac catheterization. Unfortunately — I lack further follow-up of this case beyond knowing that the patient was transferred to a referral facility, and that she was pain-free at the time ECG #3 was recorded (shown as the bottom tracing in Figure-4). I don't know the details of her medical treatment.

 

• Your thoughts on the decision not to perform emergent cath?

Figure-5: The patient was transferred to a referral center. She was pain-free on arrival at the transfer hospital.

Concluding Thoughts:

I suspect today's patient presented to the hospital with acute LMain occlusion — which then spontaneously reperfused with resolution of her chest pain. In ECG #3 — almost all acute ST-T wave changes have now resolved.

• Because of clinical improvement — emergent cath was not performed. 
• The problem with the decision not to perform prompt cath is the clinical reality that acute coronary occlusion is an evolving process. What spontaneously reopens — may just as easily spontaneously reocclude at any point in the process until the final state of infarction is reached. Given how extensive ST-T wave changes were on this patient's initial ECG — reocclusion without preventive stenting may prove fatal. 

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Acknowledgment: My appreciation to Kashif Aleem (from Lahore, Pakistan) for allowing me to use this case and these tracings. 

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ECG Blog #552 — The Leads were Not Misplaced!

The 2 ECGs in Figure-1 were obtained from the same patient. The patient had been admitted to the hospital for evaluation of abdominal pain. The repeat ECG was recorded after admission because of the sudden onset of CP (Chest Pain).

QUESTION:

• How can it be that these 2 ECGs are from the same patient?  
• NOTE: All electrode leads were correctly positioned on the patient's extremities and chest (such that the change in appearance that we see in ECG #2 is not the result of lead reversal).

Figure-1: Comparison between the 2 ECGs in today's case.

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The initial ECG in Figure-1 ...

The patient's admission ECG ( = ECG #1) is not a normal tracing.

• The rhythm in ECG #1 is sinus at a rate of ~70/minute. All intervals (PR, QRS, QTc) and the frontal plane axis are normal.
• Assuming the patient is over 35 years of age — LVH is probably present (deepest S in lead V2 + tallest R in lead V5 is very close to satisfying the 35 mm criterion, with an R wave in lead V4 that is extremely tall).
• The ST segment is coved in leads V3-thru-V6, with some ST depression and symmetric T wave inversion. There is nonspecific ST-T wave flattening in the limb leads.
• Impression: Sinus rhythm with probable LVH + ST coving and T wave inversion in leads V3-thru-V6 consistent with LV "strain" and/or ischemia. Clinical correlation is needed (and ideally finding a prior tracing for comparison).

The repeat ECG in Figure-1 ...

My 1st impression on seeing the repeat ECG was, "This is bizarre!".

• I wondered how much time had passed between the recording of ECG #1 and ECG #2?
• Seeing both tracings next to each other in Figure-1 — the differences between these 2 ECGs are striking! Not only is QRS amplitude increased in the repeat ECG — but the frontal plane axis has shifted dramatically to the right, and the QRS is now predominantly positive in lead V1 (whereas in the initial ECG — the QRS in V1 was predominantly negative). 
• This is not the result of a conduction defect — because the QRS lacks the widening of RBBB or IVCD.
• Since lead I and lead V6 are both left-sided leads — these 2 leads normally bear some resemblance to each other. Yet lead I is now predominantly negative — and left-sided chest leads V4,V5,V6 are all markedly positive.
• Yet despite this bizarre and drastic change in QRST morphology that we see between the 2 tracings in Figure-1 in both limb and chest leads — we are told that all electrode leads are correctly positioned on the patient's extremities and chest (such that the change in appearance that we see in ECG #2 is not the result of lead reversal).

How Can this Be?

• Thinking "outside the box" and remembering that the reason ECG #2 was recorded was the sudden onset of CP — I wondered about physiologic events that might cause CP, and which have been known to produce bizarre positional shifts in relative cardiac anatomy (ie, abrupt onset of pneumothorax — or since this patient was admitted for abdominal pain, perhaps intestinal perforation?).
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• OR — Could this still somehow be some manifestation of a technical misadventure?
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• PEARL #1: If some kind of “lead switch” turns out to be the cause of the bizarre change in appearance between the 2 tracings in Figure-1 — it cannot be a simple extremity electrode switch. This is because mix-up of extremity electrode placement would not affect the chest leads that now show a highly unusual and unexpected predominant R wave in lead V1. 
• Instead — any type of lead mix-up to produce the abrupt change that we see between the 2 tracings in Figure-1 would have to involve misplacement (or misconnection) of electrodes from both limb lead(s) and precordial lead(s). 

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CASE Conclusion:

• 2 hs-Troponins were negative — and another repeat ECG looked the same as ECG #2. Bedside Echo was normal, without any wall motion abnormality ==> the difference between ECG #1 and ECG #2 is not the result of acute infarction.
• Both ECGs are from the same patient.
• The 4 extremity electrodes were verified to all be on the correct extremities.
• The 6 precordial lead electrodes were all correctly placed on the chest.

The Answer:

The lead connections were incorrectly attached at the cable hub ...

• The connecting cables for unipolar lead V1 and the LL (Left Leg) electrode were swapped.
• As shown in Figure-2 — it's easy to understand how the technical misadventure of misconnecting the V1 and LL cables might happen since both cables are color-coded in RED. 
• It turns out that the cable connectors were unplugged during room cleaning — and then misconnected when the cables were reattached.

Figure-2: Magnified view of the ECG cable hub.

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Discussion:

Technical misadventures produced by limb and/or precordial lead misplacement (or misconnection) — are surprisingly common in practice, with an estimated frequency between 0.4-to-4.0% of all ECGs recorded (Sukumaran and Selvaraj — Indian Pacing Electrophysiol J 24(2):119-121, 2024 - and - Rudiger et al — Am J Emerg Med 25:174-178, 2007).

• Potential consequences of errors in lead misplacement (or misconnection) are obvious — including over- and/or under-diagnosing acute coronary occlusion.
• The most common form of lead misplacement (or lead reversal) — occurs with mix-up of 2 of the 4 limb lead electrodes. By far, the most common lead reversal is mix-up of the LA (Left Arm) and RA (Right Arm) electrodes — but any lead reversal combination is possible (See ECG Blog #479 — for a growing list of lead reversals and other technical misadventures).
• PEARL #2: Lead reversals of any 2 of the 4 limb lead electrodes are usually readily recognizable once you become familiar with the possibilities — because they generally produce characteristic patterns (as described in detail in ECG Blog #479). 
• In contrast — mix-up between limb lead electrodes and one or more of the chest lead electrodes are often unique, producing unpredictable ECG changes that complicate ECG recognition (as in today's case! ). This is because the Wilson Central Terminal is altered when there is mix-up between limb lead and chest lead electrodes.
• There is tremendous variation among ECG machines that are used worldwide. As a result — hub connections are not "standard". Fortunately — most modern ECG machines have a single cable attaching all electrodes to the machine. But some machines have 2 separate cables, providing more opportunity for lead misconnection (as seen in Figure-2).

I found the article by Paul and Jacob amazingly complete for detailing the numerous possibilities of limb lead and chest lead misplacements (Ind Pacing Electrophysiol 23(6):205-213, 2023).

• PEARL #3: Realize that although uncommon — combined mix-up between limb lead and chest lead electrodes can occur, and when it does — the resultant ECG may look bizarre with an impossible-to-explain appearance by the rules of physiology. Voltage amplitudes may be greatly increased or decreased in various leads — and unpredictable ST-T wave deviations (elevation or depression) may be seen.
• Suspect some unusual form of technical misadventure when you encounter such a bizarre tracing in a patient in whom the clinical history is not consistent with any condition likely to produce such changes (ie, normal CxR and normal Echo — especially if after verifying lead placement and repeating the ECG, the same bizarre findings are present).
• Don't forget to add checking hub lead connections to the checklist!

PEARL #4: I’ll close with reference to the primer by Lub Dub Admin — which reviews the essentials of ECG cables, including types, connectors, lead configurations and compatibility (Figure-4).

• This primer provides insight into the many ways the technical components of what goes into an ECG machine may vary. ECG machines are not all made the same. When you encounter a truly bizarre-looking ECG that does not comply with the usual predictable patterns of lead reversal — we need to put on our “detective hats” and look for unusual forms of technical misadventures.    

—  — 

Figure-3: What can go wrong with ECG Cables (by Lub Dub Admin).

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Acknowledgment: My appreciation to 林柏志 (from Taiwan) for the case and this tracing.

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ECG Blog #551 — Are there any "Normal" Beats?

I was sent the ECG in Figure-1 — told only that it was from a middle-aged man who presented for acute CP (Chest Pain). 

QUESTIONS:

• What is going on?
• How to approach interpreting this ECG?
• What is the rhythm?

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

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My Approach:

As always (assuming your patient is stable and not in need of immediately cardioversion) — I favor a systematic approach, beginning with a quick look at the rhythm ==> "Watch your Ps,Qs, and the 3Rs" (as reviewed in ECG Blog #185).

• I vary which of these 5 KEY parameters I look at first — depending on particularities of the rhythm (and depending on which of these 5 parameters are easiest to recognize).
• In today's case, as I looked at the long lead II rhythm strip — I was struck by the almost beat-to-beat variability in QRS morphology. That said — many of the beats look to be narrow, suggesting the underlying rhythm is supraventricular.
• P waves are present!

PEARL #1: The simple step of labeling P waves is often surprisingly helpful in figuring out what is going on. I have done this in Figure-2 (RED arrows highlighting those P waves that I can definitely identify).

• What do we learn from Figure-2?

Figure-2: I've labeled those P waves that I can definitely identify.

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What We Learn from Figure-2:

• The underlying rhythm in today's tracing appears to be sinus — as upright P waves with a constant and normal PR interval are seen in front of beats #1,3,4,6,8,11,13 and 15.
• I look for 2 sinus-conducted beats in a row — since if the underlying atrial rhythm is regular, seeing 2 sinus-conducted beats in a row will suggest what the P-P interval is (We see this for beats #3 and 4). The R-R interval between beats #3 and 4 is just over 3 large boxes — suggesting the presence of an underlying sinus rhythm at ~90/minute.
• NOTE: Although we do not clearly see P waves throughout the entire tracing in Figure-2 — the constant P-P interval between consecutive RED arrow P waves that we do definitely see suggests that there probably is a regular underlying P wave rhythm. 

PEARL #2: By far, the most time-effective way to interpret today's complex tracing — is to use calipers! Simply stated — I could not have determined today's rhythm with any degree of certainty without using calipers. And, by using calipers — it took me literally no more than 5 seconds to establish the conclusions that become obvious on viewing the long lead II rhythm strip that I've labeled in Figure-3:

• The underlying atrial rhythm is regular. 
• In addition to the RED arrow P waves that we definitely see — the PINK arrows in Figure-3 highlight "on time" sinus P waves that partially deform some part of the QRS.
• Even though we do not see any deformation of beat #10 — it makes sense that another "on time" sinus P wave is hidden entirely within this beat ( = the WHITE arrow drawn over beat #10).
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• PEARL #3: The PR interval for all of the "on time" PINK arrow P waves is too short to conduct normally. This establishes the presence of intermittent AV dissociation — and this proves that beats #2,5,7,14 and 16 must all be ventricular beats.
• The reason for slight variation in QRS morphology for these ventricular beats is that there is some degree of fusion between sinus-conducted P waves and the ventricular beats that follow so soon thereafter that they interrupt conduction of sinus-initiated impulses through the ventricles (See ECG Blog #128 — for more on fusion beats).
• Fusion is unlikely for beat #10 — because the "on time" WHITE arrow P wave occurs too late to be able to enter the ventricles in time to conduct. The fact that the WHITE arrow P wave arrives in the ventricles too late to conduct provides insight as to what PVCs will look like in lead II — and therefore also what PVCs will look like in simultaneously-recorded leads V1,V2,V3. 

Figure-3: Using calipers — I’ve added PINK arrows and a WHITE arrow where I expect "on time" P waves to be partially or totally hiding throughout today’s long lead II rhythm strip.

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Focus for a moment on these 4 simultaneously-recorded leads ( = leads V1,V2,V3 — and lead II in the long lead rhythm strip) For clarity — I facilitate doing this in Figure-4. 

• It should now be obvious from Figure-4 — that beat #11 looks different than the 3 other beats in leads V1,V2,V3, and in the long lead II. This is because the only normal sinus-conducted impulse among these 4 beats is this beat #11.
• Beats #9,10 and 12 are ventricular (presumably with some degree of fusion for beats #9 and 12). 

Figure-4: Focus on the 4 simultaneously-recorded leads V1,V2,V3; and on the long lead II for the purpose of highlighting QRST morphology of beats #9,10,11,12).

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Putting It All Together:

Now that we know from Figure-4 that beat #11 in the long lead II rhythm strip manifests the QRST morphology of a normal sinus-conducted beat — We can go back to Figure-3 to figure out which of the 16 beats in today's ECG are sinus conducted without partial fusion from ventricular beats:

• Beats #1,3,4,6,8,11,13 and 15 are all purely sinus-conducted.
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• PEARL #4: Assessment of ST-T wave morphology for the presence of acute ischemic changes is best done from assessment of normally conducted sinus beats.

In Figure-5 — I have selected simultaneously-conducted sinus beats in each of the 4 major lead groups (within the 4 dotted BLUE rectangles).

Figure-5: Within each of the 4 dotted BLUE rectangles — are simultaneously recorded sinus beats from each of the 4 lead groups.

To facilitate visualization of QRST morphology in each of the 4 lead groups — I have modified Figure-5 by shading out the other beats in Figure-6.

• Isn't it now much easier to appreciate marked acute ST elevation in the anterior leads? ( = beat #11 as it is seen in leads V1,V2,V3 in Figure-6)?
• Completing the pattern of Precordial Swirl that is diagnostic of acute proximal LAD occlusion (See ECG Blog #380 — for more on Precordial Swirl) — is ST depression in lateral chest leads V5,V6 (beat #13). 
• Normal sinus-conducted beats #3 and #6 reveal large Q waves with slight ST elevation in inferior leads III and aVF — and ST depression in leads I,II,aVL. There is also some ST elevation in lead aVR.

Figure-6: To facilitate visualization of acute ST-T wave changes in each of the 12 leads for sinus-conducted beats — I've shaded out other beats on this tracing.

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CASE Conclusion:

Unfortunately — I lack follow-up and the results of cardiac catheterization. Nevertheless, given the history of new CP — I feel confident in concluding the following from today's initial ECG that I have once again reproduced in Figure-7.

• The underlying rhythm in Figure-7 is sinus.
• The reason for the frequently changed QRS morphology in the long lead II rhythm strip is superimposed AIVR (Accelerated IdioVentricular Rhythm) at a rate of ~115/minute. As reviewed in ECG Blog #108 — in the setting of an acute evolving OMI, AIVR is often a "reperfusion" arrhythmia that is usually short-lived, and which usually does not require specific antiarrhythmic treatment. Instead, prompt cath with PCI is needed to prevent reocclusion of the "culprit" artery.
• The reason today's ECG is so challenging to interpret — is the frequent occurrence of fusion beats that results in constantly changing QRS morphology.
• Shading out these fusion beats (as was done in Figure-6) facilitates recognition of acute proximal LAD occlusion (Precordial "Swirl" pattern — with hyperacute anterior lead ST elevation and flattened ST depression in leads V5,V6 — as described in ECG Blog #380).
• The large inferior Q waves + ST depression in leads I,II,aVL,V5,V6 in association with ST elevation in lead aVR suggests that there may be multi-vessel disease (and/or prior inferior infarction) vs extensive LAD occlusion with "wraparound". But the message is clear ==> acute proximal LAD occlusion with immediate need for cardiac cath with PCI.

Figure-7: Today's ECG with "on time" P waves labeled. 

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Acknowledgment: My appreciation for the anonymous contribution of today's case. 

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