ECG Blog #492 — Confused by the Pacemaker

Today's patient is an older man with a permanent pacemaker that was placed ~1 year ago for complete AV Block. He presents to the ED (Emergency Department) at this time — for new CP (Chest Pain) that began earlier in the day, and which has still persisted. The patient was hemodynamically stable at the time the ECG in Figure-1 was recorded.

QUESTIONS:

• How would you interpret the ECG in Figure-1?
• Should the cath lab be activated?

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

My Thoughts on Today’s CASE:

We are told that today's patient has a pacemaker — and that he presents for new CP persisting over the course of a day. Questions that arise include the following:

• Do we see evidence of this patient's pacemaker in ECG #1?  If so — Is the pacemaker working appropriately?
• Can we assess the ECG of a patient with a pacemaker for ST-T wave changes of acute OMI? If so — Are there any worrisome findings in ECG #1?

ANSWERS: Can We Detect Acute OMI in a Paced Tracing? 

As seen in Figure-2 — Pacemaker spikes are present (within the small RED circles in leads V4,V5). Similar tiny spikes are intermittently seen in other leads.

• At least in leads V4,V5 — we see these pacemaker spikes just before wide QRS complexes with a LBBB-like morphology — so the pacmaker appears to be appropriately capturing the ventricles at ~85/minute.
• It is at least sometimes possible to assess a paced ECG for ST-T wave changes of acute ischemia. Such assessment is made more challenging by QRS widening of paced beats (and resultant altered ST-T wave morphology) — but there are times when we can see evidence of acute OMI on a completely paced tracing.
• In such instances — application of Smith-Modified Sgarbossa Criteria help to identify abnormal ST-T wave findings despite complete pacing (See Pearl #4 in ECG Blog #282 for review of Smith-Modified Sgarbossa Criteria).

PEARL #1: Even more than applying Smith-Modified Sgarbossa Criteria — I favor assessing for acute ischemia in paced tracings by looking for ST-T wave changes that just should not be there! This should be readily evident in Figure-2:

• There is no way that the 4+ mm of downsloping ST depression in lead V6 with terminal T wave positivity can be a "normal" finding (within the RED rectangle in Figure-2). If anything — we would expect secondary ST-T wave changes of LBBB or in a paced tracing to be oppositely directly to the predominantly negative QRS deflection in lead V6.
• In the context of this clearly abnormal downsloping ST depression in lead V6 — the more subtle flattened ST depression in neighboring lead V5 (BLUE arrow in this lead) is also abnormal.
• The next lead in Figure-2 to catch my "eye" — is lead V1 (within the BLUE rectangle) — as the relative amount of J-point ST elevation in this lead is clearly disproportionate to the modest size of the S wave in this lead (The relative amount of ST elevation in lead V1 does appear to satisfy the 25% criteria of Modified-Smith Sgarbossa Criteria outlined in ECG Blog #282).
• Given the clearly abnormal ST elevation in lead V1 — I thought the J-point ST elevation in neighboring lead V2 was also abnormal. While not satisfying the 25% criterion of Smith-Modified Sgarbossa — the J-point in this V2 lead is angled sharply (BLUE arrow in V2) — rather than manifesting a smoother transition as is normally expected between J-point and ST segment (Note the much smoother transition between J-point and ST segment in neighboring leads V3,V4 that I interpreted as normal).

BOTTOM Line: While the ST-T wave changes I describe above for leads V2 and V5 in Figure-2 are admittedly subtle — in this older patient with new CP — the abnormally shaped and disproportionate amount of ST depression in lead V6, supported by the disproportionate amount of ST elevation in lead V1 — has to indicate acute OMI until proven otherwise!

• PEARL #2: The presence of coved ST elevation in leads V1,V2 with clearly abnormal ST depression in leads V5,V6 is consistent with Precordial Swirl — which suggests a proximal LAD occlusion (See ECG Blog #380 for more on Precordial Swirl).
• To address the question posed at the beginning of today's case: YES, the cath lab should be immediately activated given the history of new CP and the ECG findings in Figure-2.

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

The CASE Continues:

A prior tracing on today's patient was found. To facilitate comparison in Figure-3 — I've put this previous ECG from ~8 months earlier together with today's initial ECG.

• Does availability of this prior ECG support your decision to activate the cath lab?

Figure-3: Comparison between today's initial ECG — and a previous ECG done ~8 months earlier.

Comparison with the Prior Tracing:

Availability of the prior ECG on today's patient removes all doubt about the need to activate the cath lab!

• PEARL #3: The BEST way to hone your ECG interpretation skills — is to train your "eye" in recognizing subtle findings by follow-up comparison with subsequent tracings to see how more subtle findings on the original tracing evolved over time.
• Lead-to-lead comparison between ECG #1 and ECG #2 in Figure-3 shows significant changes in virtually every lead!
• Looking first at the 2 leads that made the diagnosis for us — it is easy to see how abnormal the ST-T waves in leads V5 and V1 of Figure-1 truly were!
• Looking further at the more subtle changes in leads V2 and V5 that I highlighted above — we can confirm the validity of my observations on seeing that there was more ST elevation in lead V2 in ECG #1 than there was on the prior ECG — and the subtle, flattened ST depression in lead V5 of ECG #1 was not at all present on the prior ECG.
• ST-T wave changes in other leads are present on comparison between the 2 tracings in Figure-3 — but those changes are not nearly as easy to detect — which confirms my PEARL #4 from today's case = It is usually more difficult to assess paced tracings for acute ischemia — but it is definitely not impossible.

CASE Conclusion:

The cath lab was activated. Cardiac cath revealed the following:

• There was significant 3-vessel disease.
• 90% distal stenosis of the LMain.
• 50% mid-LAD stenosis.
• 90% patent ostial stenosis of the LCx.
• 50% mid-RCA stenosis.

The LMain narrowed area was successfully stented to the patent LAD. The patient did well in follow-up.

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PEARL #5: Had I not been told — I may not have realized that today's patient had a pacemaker from the initial ECG shown in Figure-1. Pacemaker spikes are often difficult to detect for a number of reasons:

• There could be pacemaker malfunction.
• There could be signal interference and artifact and/or "noise".
• Modern pacemakers increasingly use bipolar leads — and bipolar leads generate smaller spikes on ECG.
• Filter settings are suboptimal. This is especially true when the low-pass filter is set below the standard value of 150 Hz. That said — even at 150 Hz, the percentage of patients whose pacemaker spikes will be visible on a standard ECG has been found to be far less than the percentage for detecting pacemaker spikes on ECG with a higher low-pass filter of 300 Hz (Sun et al — Chin Med J 132(5):534-541, 2019).

Regarding Filter Settings:

I suspect suboptimal Filter settings is the most common reason that pacemaker spikes are not readily seen on many tracings. All too often — filter settings are ignored. 

• Different settings are typically used for monitoring when emphasis is placed on rhythm determination vs diagnostic mode, for which the focus is on interpreting 12-lead waveforms. 
• Greater filtering is generally used in monitor mode, with a common setting between 0.5 Hz and 40 Hz. Doing so has the advantage of minimizing artifact and baseline wander that may affect rhythm interpretation. 
• In contrast — a broader passband (typically from 0.05 Hz to 150 Hz) — is recommended for diagnostic mode, where more accurate ST segment analysis is essential.
• Modern bipolar pacemakers generate smaller pacing spike amplitudes compared to older devices, making them harder to detect on the ECG. Awareness that the filter setting is important — especially if you find yourself hopelessly looking for spikes in a tracing of a patient thought to have a pacemaker.

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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 #491 — VT until Proven Otherwise?

The ECG in Figure-1 was obtained from an older man with a history of coronary disease and chronic AFib (Atrial Fibrillation) — who was admitted acutely ill to the ICU (Intensive Care Unit) for septicemia. He was hemodynamically stable at the time this tracing was recorded.

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NOTE: The ECG in today's case looks similar to the tracing I presented a few weeks ago in ECG Blog #489. But is the answer the same?

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QUESTIONS:

• How would you interpret the ECG in Figure-1?
• How certain are you of your diagnosis?
• Did the fact that this patient was hemodynamically stable at the time this ECG was recorded influence your diagnosis?
• How would you treat this patient?

Figure-1: The initial ECG in today's case — obtained from an older man being treated in the ICU for septicemia. (To improve visualization — I've digitized the original ECG using PMcardio).

My Thoughts on Today’s CASE:

Applying the Ps, Qs and 3Rs (See ECG Blog #185) — the rhythm in Figure-1 is fast (~220/minute) — regular — with a wide QRS — and without clear sign of atrial activity. This defines the rhythm as a regular WCT (Wide-Complex Tachycardia). As per the LINKS to other cases that are found at the bottom of this page — the principal differential diagnosis is between:

• VT (Ventricular Tachycardia) — or —
• SVT (SupraVentricular Tachycardia) with either of the following: i) Preexisting BBB (Bundle Branch Block); or ii) Aberrant conduction as a result of the rapid rate.

On rare occasions — "something else" (ie, hyperkalemia, sodium channel blocker toxicity — or other toxicity) may result in a regular WCT rhythm. Given that this patient has been hospitalized in the ICU — presumably he is not hyperkalemic, such that the main consideration is to distinguish between VT vs SVT with either preexisting BBB or rate-related aberrant conduction. 

KEY Points to consider include the following:

• Statistically, in an unselected adult population — at least 80% of regular WCT rhythms without sign of atrial activity will turn out to be VT. Given that today's patient is an older adult with known coronary disease — the likelihood of VT is increased to ~90% even before we consider specific features of this ECG.
• QRS morphology may allow for greater precision in predicting WCT etiology — especially IF ECG features predictive of either VT or SVT are present. That said, even in cases in which QRS morphology is suggestive — it is rare to attain 100% certainty prior to our need to begin treatment.
• Hemodynamic stability during the WCT rhythm does not rule out VT. While true that patients with sustained VT are much more likely to decompensate than those who remain in a persistent SVT rhythm — these generalities do not always hold true. If LV function is good and the heart rate is not excessively rapid — then some patients in sustained VT may remain hemodynamically stable for a period of hours (or even longer).

What About Today's CASE?

When this case was sent to me — I found it surprising that this acutely ill patient with septicemia would be hemodynamically stable in this WCT rhythm — because the heart rate is so  very rapid (ie, ~220/minute).

• I thought the rhythm was fascicular VT — because QRS morphology resembled rbbb conduction in the chest leads (ie, with an all upright complex in lead V1 — an RS pattern in lateral lead V6 with terminal negativity consistent with rbbb-like conduction — and marked rightward axis deviation in the frontal plane).
• Given this patient's acutely ill status and the very rapid rate of his WCT rhythm — I probably would have moved to synchronized cardioversion. However, because this patient was hemodynamically stable — providers at the bedside reasonably opted for a trial of IV Amiodarone, being ready to cardiovert at any if time the patient became hemodynamically unstable.

PEARL #1: For as much as the rhythm in Figure-1 "looks" like VT — it's important to appreciate the limitations of our diagnostic accuracy from this single ECG. Confounding ECG features on this tracing include: 

• i) Lack of a clear triphasic rsR' pattern in lead V1 (instead there is an rR' pattern in lead V1 without descent of any S wave below the baseline — as illustrated in Figure-4 in the ADDENDUM below); 
• ii) Despite predominant negativity of the QRS in all 3 standard limb leads (leads I,II,III) — the lack of an all-negative QRS in either lead I and/or lead aVF means that we can not rule out a supraventricular rhythm (instead there is a tiny initial positive deflection in lead I and in each of the inferior leads); 
• iii) Lack of a completely monophasic R wave in lead aVR negates the value of this lead for predicting VT (instead there appears to be a tiny q wave = an initially negative deflection in this lead); 
• iv) Despite predominant negativity of the QRS in lateral chest lead V6 — the lack of an all negative QRS in lateral lead V6 negates the value of this lead for predicting VT (instead there is a small but-definitely-present initial R wave in this lead).

PEARL #2: Although each of the above ECG findings in PEARL #1 make a supraventricular rhythm less likely — none of them guarantee that the rhythm is VT. We need to remember that much of the time we will not be able to be certain if a regular WCT rhythm is VT or SVT at the time that we need to begin our treatment. Instead — we often need to formulate our best hunch as to what we think the rhythm is likely to be — and base our treatment decisions accordingly.

PEARL #3: Finding a prior ECG on this patient could prove invaluable — because if QRS morphology during the patient's baseline rhythm looks the same as during the WCT — this could prove that the WCT is not VT. 

• Unfortunately in today's case — this patient's baseline 12-lead ECG could not be found at the time it was needed.

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The CASE Continues:

Within minutes of beginning IV Amiodarone — the ECG shown in the bottom panel of Figure-2 was obtained. The patient remained hemodynamically stable.

QUESTIONS:

• What is learned from comparison of today initial ECG — with the repeat ECG obtained within minutes after beginning IV Amiodarone?

Figure-2: Comparison between the initial ECG — with the repeat ECG obtained within minutes of starting IV Amiodarone.

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ANSWER:

Surprisingly, the very rapid WCT rhythm seen in today's initial ECG has dramatically slowed in ECG #2 to another regular, wide rhythm.

• Comparing QRS morphology during the WCT rhythm ( = the upper tracing in Figure-1) — with QRS morphology shortly after initiation of IV Amiodarone — Isn't QRS morphology in virtually every lead remarkably similar?

PEARL #4: ECG features in ECG #2 now look much more in favor of an SVT with aberrant conduction because: 

• i) Lead V1 in ECG #2 now manifests a typical triphasic morphology for supraventricular conduction because there is a small initial r wave — followed by an S wave that descends below the baseline — that finishes with a tall, pointed terminal R' ( = a taller "right rabbit ear" ).
• ii) The tiny initial r waves that we barely saw in ECG #1 — are now much more evident (and much more consistent with supraventricular conduction with RBBB/LAHB).
• iii) Leads V4,V5 and especially V6 in ECG #2 — now manifest significantly taller narrow R waves that are strongly suggestive of a supraventricular rhythm.

KEY Point: Despite the above morphologic features of ECG #2 that strongly suggest a supraventricular rhythm — P waves are not seen! As a result — I was not yet certain that the rhythm in ECG #2 was now supraventricular.

• PEARL #5: Did you notice that the rate of the regular wide rhythm in ECG #2 is almost half that of the initial rapid WCT rhythm? — almost as if ECG #1 represented a reentry SVT rhythm, that as a result of the AV nodal blocking effect of Amiodarone — was now only conducting every-other-impulse to the ventricles.
• Alternatively — the rhythm in ECG #2 could represent junctional tachycardia with preexisting RBBB/LAHB. Although an automatic junctional tachycardia is not a common rhythm in adults — today's clinical situation (ie, a "sick" patient with multiple underlying disorders) is perhaps the most common setting in which we encounter fast junctional rhythms.

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The CASE Continues:

Since the patient remained hemodynamically stable with the rhythm in ECG #2 — IV Amiodarone was continued. A few minutes later — the rhythm in ECG #3 was observed.

• To facilitate comparison in Figure-3 — I've put the 3 ECGs in today's case together.

QUESTION:

• What do we learn from ECG #3?

Figure-3: Comparison of the 3 ECGs in today's case.

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ANSWER:

The rhythm in ECG #3 is faster than it was in ECG #2 — and is now irregularly irregular without P waves. This patient with a known history of chronic AFib — is now back in AFib with a rapid ventricular response. The 5th beat in leads V1,V2,V3 that is wider and different in morphology from the rest of the tracing is a PVC.

• Treatment of this patient with IV Amiodarone was effective! Although the end result of this treatment is still suboptimal (ie, recurrence of this patient's chronic AFib — now with a rapid ventricular response) — the "good news" is that: i) The rate of the rhythm in ECG #3 is slower than it was in ECG #1; and, ii) We now know that the rhythm in ECG #1 was not VT (because AFib is a supraventricular rhythm and QRS morphology in ECG #3 is virtually identical to QRS morphology during ECG #1).

CASE Follow-Up.

• Comparison of QRS morphology in the 3 tracings shown in Figure-1 was found to be the same as this patient's QRS morphology in prior baseline tracings. This confirms that the initial ECG in today's case was not VT. 
• Instead — today's initial rhythm most likely represents a reentry SVT in which QRS widening is the result of preexisting RBBB/LAHB.
• This patient continued to have a stormy course — but seemed to be gradually improving over time as his septicemia was treated. His AFib is chronic. Rate control will hopefully be optimized once his underlying conditions improve.
• 
  
• Editorial Comment: What I especially liked about this case — is that it keeps us humble. I truly thought the initial ECG was VT. But "not all patients read the textbook" — and over time, serial ECGs confirmed a supraventricular etiology (with preexisting RBBB/LAHB). Truly — we often have to begin treatment of wide tachycardias before we are certain of the rhythm etiology. A trial of IV Amiodarone was reasonable given hemodynamic stability of the patient — and providers were able to confirm a supraventricular etiology.

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Acknowledgment: My appreciation to Andrea D'Angelo (Naples, Italy) for allowing me to use this case and these tracings.

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ADDENDUM (8/9/2025):

Figure-4: QRS morphology in lead V1 that suggests a supraventricular etiology (from my ACLS Pocket Brain-2013).

 

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Additional Relevant ECG Blog Posts to Today’s Case: 

• ECG Blog #185 — Reviews my System for Rhythm Interpretation, using the Ps, Qs, 3R Approach.
• 
  
• ECG Blog #210 — Reviews the Every-Other-Beat (or Every-Third-Beat) Method for estimation of fast heart rates — and discusses another case of a regular WCT rhythm.
• 
  
• ECG Blog #220 — Review of the approach to the Regular WCT (Wide-Complex Tachycardia).
• ECG Blog #489 — in which the initial ECG looks similar to that in today's case (but for which the answer is different).
• ECG Blog #196 — Reviews another regular WCT.
• 
  
• ECG Blog #263 and Blog #283 — Blog #361 — Blog #384 — and Blog #460 — and Blog #468 — More WCT Rhythms ...
• 
  
• ECG Blog #197 — Reviews the concept of Idiopathic VT, of which Fascicular VT is one of the 2 most common types. 
• ECG Blog #346 — Reviews a case of LVOT VT (a less common idiopathic form of VT).
• 
  
• ECG Blog #204 — Reviews the ECG diagnosis of the Bundle Branch Blocks (RBBB/LBBB/IVCD). 
• ECG Blog #203 — Reviews ECG diagnosis of Axis and the Hemiblocks. For review of QRS morphology with the Bifascicular Blocks (RBBB/LAHB; RBBB/LPHB) — See the Video Pearl in this blog post.
• 
  
• ECG Blog #211 — WHY does aberrant Conduction occur?
• ECG Blog #301 — Reviews a WCT that is SupraVentricular! (with LOTS on Aberrant Conduction).
• ECG Blog #445 and Blog #361 — more regular WCTs.
• ECG Blog #475 — Aberrant SVT?
• 
  
• ECG Blog #323 — Review of fascicular VT.
• ECG Blog #38 and Blog #85 — Review of Fascicular VT.
• ECG Blog #278 — Another case of a regular WCT rhythm in a younger adult.
• ECG Blog #35 — Review of RVOT VT. 
• ECG Blog #42 — Criteria to distinguish VT vs Aberration.
• 
  
• ECG Blog #133 and ECG Blog #151— for examples in which AV dissociation confirmed the diagnosis of VT.
• 
  
• Working through a case of a regular WCT Rhythm in this 80-something woman — See My Comment in the May 5, 2020 post on Dr. Smith’s ECG Blog. 
• Another case of a regular WCT Rhythm in a 60-something woman — See My Comment at the bottom of the page in the April 15, 2020 post on Dr. Smith’s ECG Blog. 
• A series of 3 challenging tracings with QRS widening (See My Comment at the bottom of the page in the March 6, 2025 post on Dr. Smith's ECG Blog).
• 
  
• Review of the Idiopathic VTs (ie, Fascicular VT; RVOT and LVOT VT) — See My Comment at the bottom of the page in the September 7, 2020 post on Dr. Smith’s ECG Blog.
• Review of a different kind of VT (Pleomorphic VT) — See My Comment in the June 1, 2020 post on Dr. Smith’s ECG Blog.

 

ECG Blog #490 — Which Lead is Most Revealing?

The ECG in Figure-1 is from a young adult woman with known diabetes, who presented to the ED (Emergency Department) for a syncopal episode. The patient was alert, without chest pain, and hemodynamically stable at the time ECG #1 was recorded.

QUESTIONS:

• How would you interpret the ECG in Figure-1?
• Is the syncopal episode likely to be responsible for the abnormal findings in ECG-1 — OR — Should the cath lab be activated?

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

My Thoughts on Today's CASE:

While it is true that CNS Catastrophes may account for some of the most unusual ECG findings (See Goldberger et al — J Electrocard 47(1):80-83, 2013) — this patient's syncope (from whatever etiology this patient's syncope may have been caused by) is not the cause of the diffuse and dramatic ST-T wave changes that we see in ECG #1:

• While significant overlap of QRS complexes in a number of the leads from Figure-1 complicate assessment of ST-T wave deviations — it should be apparent that there is dramatic ST elevation in lead aVR, with equally "eye-catching" ST depression in other limb leads — and less (but still considerable) ST depression depression in all chest leads.

PEARL #1: Did YOU notice that each of the 7 QRST complexes in lead III look normal? (See Figure-2). Awareness that when there appear to be dramatic (albeit bizarre-looking) ST-T wave deflections in 2 of the 3 standard limb leads (which are leads I,II,III) — but for which the 3rd standard limb lead is "spared" from this bizarre ST-T wave morphology — the cause if these bizarre ST-T wave deflections is usually Artifact.

• We can establish with greater certainty that artifact is the cause of these dramatic (bizarre) ST-T wave changes as the result of "something" occurring in 1 of the patient's 4 extremities — IF the relative size of these abnormal deflections obeys Einthoven's Laws (See below). 

PEARL #2: Artifact is common in clinical practice. The BEST way not to overlook artifact — is to be aware of how frequently it actually occurs! I’ll suggest the following CLUES that are relevant to the presence of Artifact in today’s case:

• Clue #1: Already highlighted in PEARL #1 — in that despite unusual ST-T wave deviations in 2 of the 3 standard leads — the 3rd standard lead is spared! (and lead III is spared from artifact in Figure-2! ).
• Clue #2: The shape of the abnormal ST segments is bizarre. This unusual shape does not “fit” with the clinical situation. Although today’s patient does have diabetes — she is younger-than-usual for having an acute cardiac event — and, there is no history of chest pain (ie, Syncope without chest pain is not a common presentation of an acute MI). Finally — it’s hard to imagine that there would be this amount of ST-T wave deviation with an acute MI in a hemodynamically stable young adult who presents with syncope but no chest pain (and hard to imagine there would be this amount of ST-T wave deviation with a CNS catastrophe in an alert, hemodynamically stable patient).
• Clue #3: The bizarre ST-T wave shape in leads with ST depression (and also in lead aVR with ST elevation) — occurs at a fixed interval with respect to the preceding QRS complex (Figure-2). This tells us that whatever is producing these deflections must be related to cardiac contraction (and/or to arterial pulsation).

Figure-2: I've colored in maximal artifact deflections in RED — and lesser amplitude artifact deflections in BLUE and GREEN (See text).

KEY Clue #4: In Figure-2, we can see that the distribution of ST-T wave deflections precisely follows the location and relative amount of amplitude distortion predicted by Einthoven’s Triangle.

• The amount of ST-T wave distortion is approximately equal in 2 of the limb leads (ie, leads I and II) — and not seen at all in the 3rd limb lead (ie, no artifact is seen in lead III). By Einthoven’s Triangle (See the picture below of Einthoven's Triangle next to the link for today’s ECG Media Pearl) — the finding of equal ST segment amplitude artifact in Lead I and Lead II, localizes the “culprit” extremity to the RA ( = Right Arm) electrode.
• The absence of any artifact at all in lead III is consistent with this — because, derivation of the standard bipolar limb lead III is determined by the electrical difference between the LL ( = Left Leg) and LA ( = Left Arm) electrodes, which will not be affected if the source of the artifact is the right arm.
• As I discuss in detail in my MP-18 Audio Pearl below — the finding of maximal amplitude artifact in unipolar lead aVR confirms that the right arm is the “culprit” extremity.

  

Click on this image to hear the Audio Pearl!

—  —

 

ECG Media PEARL #18 (7:45 minutes Audio) — On recognizing Artifact — and — using Einthoven’s Triangle to determine within seconds the “culprit” extremity causing the Artifact on your ECG.

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The CASE Continues:

A short while later — the ECG was repeated (See Figure-3).

• QUESTION: How can you explain the change in appearance that we see in Figure-3 between ECG #1 and the repeat ECG #2 done ~10 minutes later?

Figure-3: Comparison between the initial ECG — and the repeat ECG recorded ~10 minutes later.

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ANSWER: The dramatic ST-T wave deviations that we saw in ECG #1 — have now totally resolved in ECG #2! Other than sinus tachycardia and some baseline artifact in a few leads — this repeat ECG is unremarkable.

• Note in particular that lead III has not changed in the repeat ECG compared to the initial tracing!
• KEY Point: It is the complete resolution of abnormal ST-T wave deflections that were seen in ECG #1 — that confirms the deflections that had been seen in ECG #1 were the result of Artifact produced by contact of the RA electrode lead with a pulsating artery (sometimes known as "PTA" = Pulse-Tap Artifact).

 

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Acknowledgment: My appreciation to Tayfun Dilek Demir (from Antalya, Turkey) for these tracings and this case.

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ADDENDUM (8/2/2025):

• For More Material — I have added this Tab on Lead Reversals & Artifact — 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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NOTE: I reproduce below in Figures 4, 5 and 6 — the 3-page article by Rowlands and Moore (J. Electrocardiology 40: 475-477, 2007) — which is the BEST review I’ve seen on the physiology explaining the relative size of artifact amplitude deflections when the cause of the artifact is a single extremity. These principles are illustrated by the colored deflections in Figure-3:

• As noted by the equations on page 477 in the Rowlands and Moore article: i) The amplitude of the artifact is maximal in the unipolar augmented electrode of the “culprit” extremity — which is lead aVR in Figure-3 (RED outline of the elevated ST segment in this lead); and, ii) The amplitude of the artifact in the other 2 augmented leads (ie, leads aVL and aVF) is about 1/2 the amplitude of the artifact in lead aVR (BLUE outline of the marked ST depression in leads aVL and aVF).
• Similarly — the amplitude of the artifact deflections in the 6 unipolar chest leads in Figure-3 is also significantly reduced from the maximal amplitude seen in leads I, II and aVR (GREEN outline of the ST depression seen in each of the 6 chest leads).

  

BOTTOM LINE: You will see artifact frequently in real-life practice. With a little practice, you can immediately KNOW with 100% certainty that the bizarre deflections on a tracing like this one are the result of artifact, and are related to arterial pulsations in one of the extremities. 

• Nothing else shows fixed relation to the QRS complex in the mathematical relationships described above, in which there is equal maximal artifact deflection in 2 of the 3 limb leads (with no artifact at all in the 3rd limb lead) — in which maximal artifact in the unipolar augmented lead will be seen in the extremity electrode that shares the 2 limb leads that show maximal artifact (as according to Einthoven’s Triangle).
• 
  
• In Other Words: When the cause of artifact originates from a single extremity — the relative amount of artifact will be: 
• Maximal in 2 of the 3 standard limb leads. 
• Absent in the 3rd standard limb lead — and ... 
• Maximal in the unipolar augmented electrode of the “culprit“ extremity (which as per the RED outline in Figure-3 — is lead aVR). 
• 
  
• PEARL #3: Appreciation of these electrophysiologic principles allowed me to instantly identify lead aVR as the “culprit” extremity in today’s case — because this is the augmented lead with maximal artifact!

 

Figure-4: Page 475 from the Rowlands and Moore article referenced above (See text).

 

Figure-5: Page 476 from the Rowlands and Moore article referenced above (See text).

 

Figure-6: Page 477 from the Rowlands and Moore article referenced above (See text).