EXTRA COPY- ECG Blog #527 — What’s Going On? — EXTRA COPY

The ECG in Figure-1 — was obtained from an older man who presented for care with new CP (Chest Pain).

QUESTION: 

• Should the cath lab be activated?

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

MY Thoughts:

It is tempting on first glance at today's tracing from this patient with new CP — to be very concerned by the marked ST segment deviation. And then — I looked closer at lead I:

• PEARL #1: Compared to the other 11 leads in this tracing — the QRST complex in Lead I looks almost normal (with no more than subtle nonspecific ST-T wave flattening in this lead). My favorite Clue to the presence of Artifact as the cause of marked, bizarre complexes in many (most) other leads — is that one of the 3 standard leads looks relatively normal. And despite dramatic (and bizarre) ST-T wave deflections in the other 2 standard leads ( = leads II and III in Figure-1) — the ST-T wave in lead I looks to be relatively unaffected!

PEARL #2: As discussed in ECG Blog #201 — The distribution of the bizarre ST-T wave deflections seen in Figure-1 — precisely follows the location and relative amount of amplitude distortion predicted by Einthoven’s Triangle.

• That is — the relative amount of bizarre ST elevation is approximately equal in 2 of the 3 standard limb leads (ie, in leads II and III) — but it is not seen at all in the 3rd standard limb lead (ie, there is no artifact seen in lead I). By Einthoven's Triangle (See the picture of Einthoven's Triangle just below today’s ECG Media Pearl) — the finding of equal ST segment amplitude artifact in lead II and lead III, localizes the "culprit" extremity to the LL ( = Left Leg) electrode.
• The absence of any artifact at all in lead I is consistent with this — because, derivation of the standard bipolar limb lead I is determined by the electrical difference between the RA ( = Right Arm) and LA ( = Left Arm) electrodes, which will not be affected if the source of the artifact is the left leg.
• As I discuss in detail in my Audio Pearl below — the finding of maximal amplitude artifact in unipolar lead aVF confirms that the left leg is the “culprit” extremity. 

—  —

 

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.

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

PEARL #3: Another KEY Clue to the presence of artifact — is if you are able to see undisturbed continuation of the underlying rhythm despite the artifact! Figure-2 shows how this is possible in today's case:

• There are actually 2 artifact deflections within each R-R interval in today's initial tracing (alternating BLUE and YELLOW arrows in lead aVL of Figure-2). These are seen as dual positive deflections within each R-R interval in all limb leads except lead I — and as dual negative artifact deflections within each R-R interval in the 6 chest leads.
• Focusing on the QRS complex in lead I that is unaffected by artifact — I've added a RED time-line parallel to the ECG grid line that exends through simultaneously-recorded leads II and III — with this time-line marking the beginning of the QRS complex that we can clearly see in lead I.
• I've also added a BLUE time-line that marks the end of the QRS in lead I. Thus, we can see that the QRS complex in lead I lies in between the RED and BLUE lines. This allows us to follow these RED and BLUE lines to know where to look for other "on time" partially hidden QRS complexes in simultaneously-recorded leads (and at least in lead III — we can identify a small "on time" rS complex between these 2 time-lines).
• I've added similar RED and BLUE lines to lead aVL — which suggests that very small, subtle underlying "on time" QRS deflections continue for most beats in simultaneously-recorded leads aVR and aVF.
• The presence of continuous "on time" QRS complexes is of course much easier to see in the chest leads — because the predominantly negative artifact complexes occur after the QRS, and therefore do not hide the QRS.
• 
  
• NOTE: The reason the RED and BLUE lines that I've added in Figure-2 are not "vertical" — is that this ECG is from a screen shot, in which angulation has been introduced that results in some distortion. But these colored lines are parallel to the heavy grid lines — such that the timing of complexes in simultaneously-recorded leads is accurate.

Figure-2: I've added colored time lines in simultaneously-recorded limb leads in today's initial ECG.

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

The CASE Continues:

Artifact was suspected in today's case. As a result — providers took off, and then reapplied the electrode leads. They then recorded the repeat ECG that is shown below in Figure-3. Your impression?

Figure-3: I've put today's 2 tracings together to facilitate comparison. The repeat ECG (bottom tracing) was recorded after reapplication of electrode leads.

My Thoughts on Figure-3:

After repositioning the electrode leads — the artifact seen in ECG #1 has completely resolved!

• The artifact in ECG #1 was the result of PTA = Pulse-Tap Artifact (See below). 
• ECG #2 confirms that the tiny deflections seen in between the RED and BLUE time-lines in simultaneously-recorded in leads III, aVR and aVF — did indeed represent underlying "on time" QRS complexes that had been partially hidden in these leads.
• ECG #2 shows us the reason the QRS complex in lead II was so hard to see in the initial ECG — namely that after resolution of artifact in ECG #2, we see how tiny the isoelectric QRS in lead II truly is.
• We also see that the very small rS shape of the QRS that we identified in lead III of ECG #1 is comparable to the shape of the QRS in this lead after resolution of artifact.

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

PTA (Pulse-Tap Artifact):

As emphasized by Samaniego et al (Emerg Med J 20:356-357, 2003) — there are 2 main sources of artifact, which are "physiologic" vs "non-physiologic" sources.

• Non-Physiologic Artifact Sources — include 60 hertz cycle interference (from AC current devices in the area) — and/or cable or electrode malfunction (ie, loose or broken wire, loose electrode lead connection, etc.).
• Physiologic Artifact Sources — include patient movement and/or voluntary or involuntary muscular activity (ie, tremor, shivering, scratching, coughing, hiccups, distressed breathing — and PTA, among others).

Pulse-Tap Artifact — is physiologic, as it is caused by electrode contact with a pulsating artery in one of the 4 extremity electrodes. Since arterial pulsations are the result of cardiac contraction — PTA occurs at a fixed interval with respect to each preceding QRS complex.

• The 1st time I saw PTA on an ECG — I did not know what this phenomenon was. Since that time — I've seen numerous cases (See ECG Blog #201 — ECG Blog #490 — with more examples of PTA from Dr. Smith's ECG Blog, as shown on my Lead Reversal-Artifact Page). 
• The "good news" is that once you become aware of PTA — you'll be able to instantly identify it by the geometric relationships it produces, as validated by Einthoven's Triangle (as I discussed above for today's case — and reinforce below in today's ADDENDUM).

PEARL #4: The above said — today's case is unique because instead of seeing a single artifact deflection related by a fixed interval to each preceding QRS complex in 2 of the 3 standard leads — we see 2 artifact deflections with each beat! (as per the alternating BLUE and YELLOW arrows in lead aVL of ECG #1 in Figure-3).

• Prior to today's case — all the examples of PTA that I had encountered only a single artifact deflection with each beat.
• However, as shown in today's case — PTA may manifest 2 separate deflections within each R-R interval. This is because the mechanical motion of the pulsating artery may contact the overlying electrode twice during each cardiac cycle ( = Once when the artery expands, as it does during systole — and a 2nd time when the artery relaxes in diastole).

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

Acknowledgment: My appreciation to Bashiruddin Sayeem (from Chittagong, Bangladesh) for the case and this tracing.

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

 

ADDENDUM (4/XXX/2026):

To reinforce the concepts that facilitate instant recognition of the "culprit" extremity causing PTA — I've reproduced in Figure-4 the illustration I developed for My Comment that can be found at the bottom of the page in the September 15, 2023 post in Dr. Smith's ECG Blog.

How to Recognize PTA within Seconds!

Look first at the TOP tracing in Figure-4. The bizarre deflections in multiple leads immediately suggest some form of artifact.

• We know we are looking at artifact in this TOP figure — because despite marked distortion of the QRST in leads II and III — the 3rd standard limb lead ( = lead I) is not affected by artifact!
• We know that this artifact is physiologic and related to the cardiac cycle because of the fixed distance of this artifact after each QRS complex (best seen in the long lead II rhythm strip).
• We also know this artifact is the result of a single "culprit" extremity — because it follows the rules set forth by Einthoven's Triangle.

To facilitate recognition of these Einthoven Triangle rules — I've labeled the BOTTOM tracing in Figure-4 — and have once again added the lead derivations of Einthoven's Triangle (in Figure-5 below).

• Lead I is unaffected by artifact (within the RED rectangle).
• Maximal artifact is seen in the other 2 standard limb leads ( = Leads II and III) — as well as in that augmented lead that is common to both of these maximal artifactual limb leads (in this case lead aVF, that is placed on the LL = Left Leg extremity — with these 3 leads [ = leads II,III,aVF] showing maximal artifact, as shown within the BLUE rectangles in Figure-4).
• 
  
• PEARL #5: It is by looking for that augmented lead that shows maximal artifact — that allows us to instantly identify the "culprit" extremity ( = the LL = Left Leg electrode in today's case).
• The other 2 augmented leads ( = leads aVR and aVL — within the GREEN rectangles) — show approximately half the amount of artifact, compared to the maximal artifact seen in leads II,III,aVF.
• Final confirmation that the only thing that can produce these mathematical relationships is PTA — is forthcoming from seeing a lesser amount of artifact in each of the chest leads (approximately 1/3 the amount of artifact, as shown within the YELLOW rectangles).
• 
  
• BOTTOM Line: It literally took me no more than seconds to recognize PTA in today's initial tracing because: i) Despite bizarre deflections in multiple leads — I immediately saw a normal-looking lead I; — and, ii) I saw maximal artifact in the other 2 standard limb leads ( = leads II,III) — with the fact that the augmented lead showing maximal artifact was lead aVF telling me to look at the left Foot (the LL electrode) for the source of the PTA.

Figure-4: Example of PTA excerpted from My Comment in the September 15, 2023 post in Dr. Smith's ECG Blog.

Figure-5: Using Einthoven's Triangle to determine within seconds the "culprit" extremity of the artifact on your ECG.

 ==================================

 

Beyond-the-Core: 

I reproduce below in Figures 6, -7 and -8 — 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 above by the deflections within the colored rectangles in Figure-4.

• 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 aVF in Figure-4; and — ii) The amplitude of the artifact in the other 2 augmented leads (ie, leads aVR and aVL) is about 1/2 the amplitude of the artifact in lead aVF (within the GREEN rectangles in Figure-4).
• Similarly — the amplitude of the artifact deflections in the 6 unipolar chest leads in Figure-4 is also significantly reduced from the maximal amplitude seen in leads II, III and aVF (within the YELLOW rectangles in each of the 6 chest leads).
• 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).

 

Figure-6: Page 475 from the Rowlands and Moore article referenced above (See text).

 

Figure-7: Page 476 from the Rowlands and Moore article referenced above (See text).

 

Figure-8: Page 477 from the Rowlands and Moore article referenced above (See text).

 

EXTRA COPY — ECG Blog #528 — What's the Rhythm? Why? — EXTRA COPY

XXXXXX

XXXXXXX

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

XXXXXX

Figure-2: I've labeled today's ECG.

XXXXXX

Figure-3: Laddergram of today's rhythm.

XXXXXX  

XXXXXXX

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

GREAT post on FB from Cardiology Notes (on Facebook !!! )
—  YES — I can acknowledge them as “Cardiology Notes” — and perhaps I should give the link to this post on FB?
— Also to acknowledge — Omar Hassan and Khaled Ash (both from FB !!! )
 
TITLE of MY BLOG POST —
 — “The Patient just left … “
 
THIS IS THE CASE from Cardiology Notes:
https://www.facebook.com/good.job.692776/posts/pfbid0gY4XyPWXBYniYjdLoifq7oPJji2sMU8V7G3d1jAgd5nmUbyuRa8LRZitH7RZqCArl
 
A 54 year old female patient with history of ischemic heart disease complaining of palpitations and dyspnea
MY 1stt REPLY:
FASCINATING rhythm! I've taken the figure posted by Khaled Ash (above) — and have added light BLUE arrows that to me suggest 1:1 retrograde V-A conduction (in addition to the suggestion of 3:2 Wenckebach conduction!
Possibilities are several — in addition to AIVR with 3:2 Wenckebach conduction out of the ventricular focus — this could be junctional with a baseline ECG showing MBBB ( = Masquerading Bundle Branch Block), again with 1:1 VA conduction backward and 3:2 Wenckebach out of the AV node.
My PLEA to Cardiology Notes — PLEASE GIVE US FOLLOW-UP of this fascinating case! Surely YOU have some follow-up!
— What does the baseline ECG look like?
— Is this patient on Digoxin? (if so — likely Dig Toxicity)
— What happened? (Recent acute MI? Electrolyte abnormalities?)

 
MY 2nd REPLY:
NOTE: Cardiology Notes and Omar Hassan, Khaled Ash and myself have all been corresponding about this fascinating case. The patient is on Respiridone (See attached — as this psychotropic medication IS associated with a number of adverse effects that may have contributed to this unusual cardiac arrhythmia !!!
Otherwise — Cardiology Notes has shared with us that this patient signed out of the hospital on his own, refusing further evaluation. Pt was not cooperative !!! — but at least he felt well enough to sign out AMA on his own !!!
I would have loved to see a copy of his previous ECG to help determine if today's rhythm is supraventricular (with MBBB) vs ventricular in etiology as a possible adverse effect from Respiridone ...
 
Respiridone — high risk of sudden death
Ray et al — N Engl J Med 360(3):225-235, 2009
https://pmc.ncbi.nlm.nih.gov/articles/PMC2713724/
 
Users of typical antipsychotics have increased risk of serious ventricular arrhythmias and sudden cardiac death. However, less is known regarding the cardiac safety of the atypical antipsychotic drugs, which have largely replaced the older agents in clinical practice.
 
At present, less is known regarding the cardiac safety of the atypical antipsychotic drugs, which have largely replaced the older agents in clinical practice. Several atypical antipsychotics block repolarizing potassium currents² and prolong ventricular repolarization,^1,13 and the electrophysiologic effects of some drugs are comparable to those of the older agents. However, although torsade de pointes has been reported with atypical antipsychotics,^14–16 whether these drugs increase the risk of sudden cardiac death to the same extent as the older medications is unknown. We thus conducted a large retrospective cohort study designed to compare the risk of sudden cardiac death for the two classes of antipsychotic drugs.
 
Our study did not assess the mechanisms by which either class of antipsychotics increased risk of sudden cardiac death. Although antipsychotics have chronic adverse cardiovascular effects,¹² the risk of sudden death was elevated in an analysis excluding long-term users, which suggests that acute drug effects are involved. We believe the most plausible explanation is that antipsychotic drugs increase the risk of serious ventricular arrhythmias, probably through blockade of potassium channels and prolongation of cardiac repolarization. However, other mechanisms may be involved, including autonomic effects, inhibition of other ion channels, or other acute cardiotoxicities, such as the myocarditis associated with clozapine use.³⁸
In conclusion, current users of both typical and atypical antipsychotics in the study cohort had a similar dose-related increased risk of sudden cardiac death. This suggests that with regard to this adverse effect, the atypical antipsychotics are no safer than the older drugs.
Respiridone does prolong the QTc — but unless there is an overdose, usually by not enough to cause Torsades — it may cause bradycardia — it may cause av block (although this is less common at lower doses.

EXTRA COPY — ECG Blog #526: Epigastric Pain — EXTRA COPY

The ECG in Figure-1 — was obtained from a younger adult male who presented to the ED (Emergency Department) with new epigastric pain. The patient had a history of prior PCI (Percutaneous Coronary Intervention).

• The cardiology team was consulted — but felt there was no indication of a STEMI, and that the tall chest lead T waves represented a repolarization variant in this patient whose presenting symptom was abdominal pain.

QUESTIONS:

• Do YOU agree with the cardiology consultant's opinion?
• What would you do? 

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

MY Thoughts:

It’s always challenging when you disagree with your consultant and the patient’s well-being is dependent on a timely correct diagnosis. There are many reasons why the Cardiology Team’s opinion is not correct. These include: 

• i) The “focus” is wrong. In a patient who presents to the ED for new-onset of a potential “CP (Chest Pain) Equivalent” symptom — the onus is on medical providers to rule out an acute event, rather than having to “rule it in”. (This is especially true in a patient with known coronary disease, given prior PCI).
• ii) The diagnosis of a “repolarization variant” — is a diagnosis of exclusion (ie, to only be made after you have ruled out the possibility of an acute event). While I have seen very tall, peaked, non-hyperkalemic T waves represent a benign repolarization variant — this is rare! Instead — the presence of overly tall, peaked chest lead T waves in a patient who presents to the ED with new symptoms should be suspected as representing a form of deWinter-like T waves until proven otherwise (See the ADDENDUM below).  
• 
  
• iii) The morphology of the chest lead ST-T waves is diagnostic! As shown below in Figure-2 — these T waves are symmetric (Benign repolarization variants tend to be asymmetric — with slower rising and more rapid downsloping of the ascending and descending T wave limbs). In addition — the T wave peaks become “fatter”-than-they-should-be” as one more toward chest leads more lateral than lead V3. Finally — straightening of the ST segment takeoff in lead V6 indicates hyperacuity in a patient with new symptoms.
• iv) STEMI Criteria are satisfied in Figure-2 (ie, the dotted RED lines in leads V4,V5 show 2 mm of J-point ST elevation). To Emphasize: STEMI criteria are not needed to justify the need for prompt cath in today’s patient — but these criteria are nevertheless satisfied.
• v) Limb lead findings confirm that today’s ECG is not a repolarization variant! This is because: a) There is clearly abnormal ST segment straightening with angulation of the T wave onset in leads III and aVF (These represent subtle “reciprocal” changes to the chest lead T wave peaking); — and, b) There is equally subtle-but-real ST elevation in lead aVL — and — a “bulky” (hyperacute) T wave in lateral lead I.

Bottom Line: In a patient who presents to the ED with new symptoms — today’s ECG is strongly suggestive of acute LAD occlusion (LAD OMI) until proven otherwise! 

Figure-2: I've labeled today's ECG.

What to Do?

If your cardiology consultant does not agree with your interpretation — Consider the following:

• Repeat the ECG within 10-20 minutes! Especially in the presence of ongoing symptoms — it is often surprising how quickly acute ECG finding may evolve. Seeing “dynamic” ST-T wave changes in a patient with new symptoms should serve to convince the most skeptical of interventionists of an acute evolving event in need of prompt cath.
• And, if your 1st repeat ECG fails to show significant changes — Continue to order timely additional repeat tracings (which in a patient with ongoing symptoms will usually show changes).
• Find a prior ECG for comparison! Given the history of previous PCI — We know that this patient has previous ECGs. If the ECG in Figure-2 represents a new acute event — there is no way that a previous ECG will show such overly tall, peaked T waves (ie, You can immediately prove that the ST-T wave changes in Figure-2 are new if these findings are not seen on a previous tracing).
• Perform bedside Echo. If your patient who shows the extensive ECG abnormalities seen in Figure-2 continues to have ongoing symptoms — a bedside Echo will almost always show a localized wall motion abnormality that is diagnostic of an acute event.
• Realize that any elevation in Troponin is significant in a patient with persistent new symptoms. 

To Emphasize: Waiting for serum Troponin to rise takes longer than the time it should take to repeat the ECG, find a prior tracing (if PCI was done in the same hospital) — and/or do bedside Echo. 

• CAVEAT #1: As noted in ECG Blog #508 — Although one may be momentarily comforted by an initial normal hs-Troponin value — this in no way rules out an acute cardiac event. Wereski et al (JAMA Cardiology, 2020) — found that 14% of patients with an acute STEMI had a normal initial hs-Troponin (and ~25% had hs-Troponin levels below the infarction “rule-in” level). 
• Therefore — IF serial ECGs show "dynamic" ST-T wave changes — or, a prior ECG looks different — or, bedside Echo shows a localized wall motion abnormality — then waiting for an elevated Troponin wastes precious time (and precious myocardium).
• 
  
• CAVEAT #2: Bedside Echo is only helpful in lowering the likelihood of an acute event IF: a) LV contractility is completely normal; and, b) The patient is having symptoms at the time the Echo is done (Nothing is ruled out if the patient is pain-free at the time the Echo is done).

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

CASE Follow-Up:

• Bedside Echo showed reduced contractility.
• The patient continued to have severe pain.
• As a result — cardiac cath was performed and showed a "culprit" lesion in the LAD (Left Anterior Descending) coronary artery. The patient's pain was relieved following PCI — and he has done well in follow-up.

================================== 

Acknowledgment: My appreciation to Nirdosh Rassani (from Quetta, Pakistan) for the case and this tracing.

==================================  

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

ADDENDUM (4/4/2026): 

• See ECG Blog #183 for review of the original 2008 NEJM manuscript by deWinter and colleagues.
• ECG Blog #341 is equally insightful (There are many other examples of deWinter-like T waves on this Blog).

MY Observations regarding De Winter T Waves: 

Over the past decade — I have observed literally hundreds of cases in numerous international ECG-internet Forums of deWinter-like T waves in patients with new cardiac symptoms.

• Many (most) of these cases do not fit strict definition of “de Winter T waves” — in that fewer than all 6 chest leads may be involved — J-point ST depression is often minimal (if present at all) in many of the chest leads — and, giant T waves are limited.
• ECG changes in many of these cases are not “static” until reperfusion, as was initially reported in 2008 by de Winter et al. Nevertheless, cath follow-up routinely confirms LAD occlusion.
• 
  
• MY "Take": I believe there is a spectrum of ECG findings, that in the setting of new-onset cardiac symptoms is predictive of acute LAD occlusion as the cause. What will be seen on the ECG depends greatly on when during the process the ECG was obtained. While many of these patients do not manifest “true de Winter T waves” (because their ECG pattern does not remain static until reperfusion by coronary angioplasty) — for the practical purpose of promptly recognizing acute OMI — I don’t feel ( = my opinion) that it matters whether a “true” de Winter T wave pattern vs simple “hyperacute” T waves (that are deWinter-like) is present.

 

—  —

TODAY’s ECG Media PEARL #1 (3:00 minutes Audio): — relates to the phenomenon of deWinter-like T waves.