EXTRA COPY- ECG Blog #529: Should Prompt Cath be Done? (4-21.1-2029) - EXTRA COPY

The ECG in Figure-1 was obtained from an older woman — who presented following an episode of severe epigastric pain, associated with nausea, vomiting and dyspnea. This ECG was obtained a number of hours after the episode had subsided.

QUESTIONS:

• How would YOU interpret the ECG in Figure-1?
• Should you activate the cath lab?  

Figure-1: The initial ECG in today's case — obtained from an older womman following an episode of severe epigastric pain. (To improve visualization — I've digitized the original ECG using PMcardio).

My Thoughts:

The ECG in Figure-1 shows a fairly regular sinus rhythm at ~90/minute. The PR and QRS intervals are normal — and the QTc is at most borderline prolonged. The frontal plane axis is normal at about 0 degrees. There is no chamber enlargement.

Regarding Q-R-S-T Changes:

• Q Waves: None.
• R Wave Progression: Delayed. Transition (where the R wave becomes taller than the S wave is deep) does not occur until between lead V5-to-V6. That said — at least a small R wave is present in each of the chest leads, with gradual increase in R wave size until transition occurs.

Regarding ST-T Wave Changes:

As highlighted in Figure-2 — ST-T wave appearance is clearly of concern — with abnormal findings in almost all leads.

• ST segments in multiple leads are flat. Most remarkable is the shelf-like ST depression that is maximal in leads V2,V3,V4 (within the RED rectangle in Figure-2). 
• A lesser degree of flat ST depression is seen in the remaining chest leads (ie, in leads V1;V5;V6).
• There is terminal T wave positivity in all 6 chest leads.

In the Limb Leads:

• There is nonspecific ST-T wave flattening with slight depression in high-lateral leads I and aVL (BLUE arrows in these leads).
• In the inferior leads — leads II and aVF show nonspecific ST-T wave flattening. KEY Point: The 3rd inferior lead (which is lead III) — shows ST segment coving, with a hint of ST elevation.
• The remaining limb lead (which is lead aVR) — shows a very slight amount of ST elevation. 

My Impression: 

If today's patient had presented with the ECG in Figure-2 and a history of new-onset chest pain — then this tracing would be especially worrisome.

• Instead — this patient presented with severe epigastric pain, associated with nausea, vomiting and dyspnea. That said — in view of the fact that the symptoms reported could represent a CP (Chest Pain) “equivalent” symptom — Consideration has to be given to the possibility of an acute ongoing cardiac event.
• ST depression is seen in 8/12 leads in Figure-2 (leads I,aVL; and the 6 chest leads). Even without any more than the minimal ST elevation in lead aVR — these findings suggest DSI (Diffuse Subendocardial Ischemia). As discussed in ECG Blog #483 and ECG Blog #400 — DSI may be the result of either non-cardiac causes (ie, anemia, GI bleeding, marked hypotension, "sick" patient, etc.) — or — significant coronary disease, which could be acute.
• As suggested by the RED arrows (within the RED rectangle in Figure-2) — ST depression appears to be maximal in leads V2,V3,V4 — which strongly suggests the possibility of acute or recent posterior OMI.
• In this context — the ST segment coving with slight ST elevation in lead III could reflect associated inferior OMI in the setting of underlying multi-vessel disease (ie, similar to an Aslanger Pattern — as described in detail at the bottom of this page).
• 
  
• BOTTOM Line: Although more information is clearly needed to better define what is going on — one needs to consider the possibility of an acute occlusion infarction (ie, an "OMI") until proven otherwise.

Figure-2: I've highlighted key findings in today's ECG.

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CASE Follow-Up:

Clinical details are unfortunately lacking in today's case. That said, from what I am aware of — the possibility of an acute MI was not considered until a serum Troponin came back markedly elevated.

• At that point — the MI was declared a NSTEMI (Non-ST Elevation Myocardial Infarction). In the absence of ST elevation — cardiac catheterization was deemed to be "not necessary".
• An Echo was not done until later. It showed an inferolateral wall motion defect with significant LV dysfunction. At this point — cardiac cath was finally recommended, but not performed because the patient refused the procedure.
• The patient's condition deteriorated — but with full informed consent, she still refused cardiac cath. Eventually, after a complicated hospital course — her condition improved and the patient was discharged from the hospital.
• The patient never underwent cardiac catheterization ( = her informed consent decision not to undergo cath). A number of weeks later on follow-up — she appeared stable on her new medical treatment regime for heart failure. We can only wonder if the heart failure resulting from this patient's extensive infarction might have been prevented had prompt cath with PCI been done.

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COMMENT:

There are lessons-to-be-learned from this case.

• It is well established that not all patients with an acute MI have CP (Chest Pain). Instead, some patients have other "CP-equivalent" symptoms (ie, epigastric pain, dyspnea) — while others have no symptoms at all (See ECG Blog #228).
• That today's patient had a recent (ongoing) MI was not appreciated until her Troponin came back markedly elevated. This possibility should have been realized as soon as her initial ECG (shown in Figure-1) was recorded. Yet a few days passed before this possibility was considered.
• Given the less typical presentation (ie, epigastric rather than chest pain) — I would interpret today's initial ECG as suspicious but non-diagnostic. The diffuse ST depression (present in 8/12 leads in Figure-2) — clearly indicates DSI (Diffuse Subendocardial Ischemia). As noted above — DSI often (but not always) indicates severe underlying coronary disease.

The situation of having to determine if a patient with a non-diagnostic initial ECG is having an acute MI is common. 

• "Time is Muscle (myocardium). If the cause of an acute MI is acute occlusion of a major coronary vessel (ie, an "OMI" = Occlusion-associated Myocardial Infarction) — then we need to appreciate that the more time that passes until the occluded vessel is reperfused (either by cardiac cath with PCI or by use of thrombolytic agents) — the greater the amount of myocardium that will be lost.
• As repeatedly shown in Dr. Smith's ECG Blog (See My Comment in the February 8, 2026 post) — the most benefit from reperfusion occurs within the first 4 hours after acute coronary occlusion (and every 2-hour delay results in up to 60% more myocardium infarcted).

There are 2 main types of acute myocardial infarction: 

• Type 1 MI's — which are caused by a ruptured plaque that results in acute occlusion of a major coronary vessel. 
• Optimal treatment of Type 1 MI's consists of reopening the acutely occluded artery (ie, reperfusion by cardiac cath with PCI — or with use of thrombolytic agents). 
• Sometimes (if not often) — the acutely occluded artery may spontaneously reopen (which is why the patient's symptoms and ECG abnormalities may suddenly improve — even before any treatment is given).
• But what spontaneously reperfuses — may just as easily spontaneously reclose (which is why with a Type I MI, even if symptoms and the ECG suddenly improve [or completely resolve] — definitive treatment with PCI may still be needed to prevent reclosure).

• Type 2 MI's — which are not the result of a ruptured plaque, but instead are due to an oxygen supply-demand mismatch (which may be seen with "high-demand" states, in which the heart requires more oxygen than it receives — as may occur with marked stress states, septicemia, severe anemia, sustained tachyarrhythmias, or shock, among other causes).
• Optimal treatment of Type 2 MI's is to find and "fix" the cause of the supply-demand mismatch (Neither PCI nor thrombolytics benefit a Type 2 MI).
• If it is not clear from history and serial ECGs — then cardiac cath may occasionally (not often) be needed to distinguish between a Type 1 vs Type 2 MI.

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Is "NSTEMI" a Useful Term?

The reason today's ECG was called a NSTEMI (Non-ST Elevation Myocardial Infarction) — is because Troponin was significantly elevated, but no ECG satisfied sufficient millimeter-based ST elevation criteria to qualify as a STEMI.

• It was on this basis (ie, that no STEMI was present) that the recommendation for acute cardiac catheterization was delayed for more than a day. As discussed above — the patient consistently refused cardiac cath — so this delay did not influence the ultimate outcome. That said — it is nevertheless important to consider WHY the recommendation for cardiac cath was so greatly delayed.
• Practically speaking — the diagnostic designation, "NSTEMI" — serves no useful purpose. On the contrary — the "default diagnosis" of calling cases such as the one in today's post a NSTEMI is not only without utility — But it is potentially harmful — because for clinicians who are "stuck" in the outdated STEMI Paradigm, declaring that an MI is a "NSTEMI" provides a false sense of security that prompt cath with PCI is not needed — and this all-too-often results in significant delay until cardiac cath is finally done (and as stated above, "Time is Muscle" = lost myocardium).
• The Clinical Reality: Up to 35% of "NSTEMIs" are found (on their delayed cath) to have had acute coronary occlusion despite a lack of ST elevation on one or more ECGs (Aslanger, Smith et al- IJC Heart & Vasculature, Vol. 30, 2020 — Chi-Sheng Hung et al- Critical Care 22:34, 2018 — Khan et al- Eur Heart J 38(41): 3082-3089, 2017 — and — Avdikos, Michas, Smith- Arch Acad Emerg Med 10(1), 2022).
• And even in those cases in which STEMI criteria are eventually met: i) Waiting for ST elevation to finally develop often results in a delay of too many hours (with loss of too much myocardium); — and, ii) As documented in many cases on Dr. Smith's ECG Blog — for many of these slow-to-develop STEMI cases, the provider still somehow ends up writing "NSTEMI" on the discharge diagnosis.

BOTTOM Line: The millimeter-based "STEMI Paradigm" is flawed — because it misses at least 25% of acute coronary occlusions (which is the group of acute MI's that we care about — because these are the MI's that benefit from prompt reperfusion by either cath with PCI or with thrombolytics). 

• We would all be better served if the outdated and misleading term, "NSTEMI" — was no longer accepted as a diagnosis.
• We would be BEST served if instead of insisting on millimeter-based ST elevation criteria before considering cath with PCI or thrombolytics — if we instead adopted those ECG and clinical clues that have been shown to predict acute coronary occlusion (ie, an acute OMI) without having to wait for sufficient ST elevation (that might never come) before doing so (See detailed discussion in my ECG Blog #337 — in the July 31, 2020 Dr. Smith post — as well as in numerous additional posts in this ECG Blog and in Dr. Smith's ECG Blog).

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What is Aslanger's Pattern?

I introduced the concept of Aslanger's Pattern in ECG Blog #258 and ECG Blog #322. The premise of Aslanger's — is that IF there is inferior MI + diffuse subendocardial ischemia — then the vector of ST elevation will shift rightward. This results in:

• ST elevation in lead III (as a result of the acute inferior MI) — but not in the other inferior leads (II, aVF) because of the rightward shift in the ST elevation vector.
• ST depression in one or more of the lateral chest leads (V4, V5, V6) with a positive or terminally positive T wave — but without ST depression in lead V2. (Marked ST depression from multi-vessel coronary disease serves to attentuate what would have been ST elevation in leads II and aVF).
• ST elevation in lead V1 that is more than any ST elevation in lead V2.
• There may be more reciprocal ST depression in lead I than in lead aVL (because of the rightward ST vector shift).
• The only leads showing significant ST elevation may be leads III, aVR and V1 (reflecting the inferior MI + subendocardial ischemia from diffuse coronary disease). 

Regarding Today's CASE:

The ECG in Figure-2 does not satisfy all of the above features of Aslanger's Pattern (ie, Instead of ST elevation in leads V1 and V2 — there is ST depression in these leads). That said — the elements of today's case that do resemble this pattern are:

• There is DSI (Diffuse Subendocardial Ischemia).
• The ST segment is coved and slightly elevated in lead III, but not in the other inferior leads.

Bottom Line: Today's patient presented with severe new-onset symptoms potentially consistent with a "CP-equivalent" syndrome. The initial serum Troponin was markedly elevated — thus confirming an acute MI. 

• ST depression is maximal in leads V2,V3,V4 — suggesting an acute posterior OMI (and acute posterior OMI is very commonly associated with acute inferior involvement).
• The diffuseness of ST depression in Figure-2 suggests severe underlying coronary disease.
• In this context, although not strictly satisfying all features of Aslanger's Pattern — I interpreted the ST coving and slight elevation in lead III as suggestive of acute inferior involvement.
• Regardless — Given the history and the markedly elevated initial Troponin — indication for prompt cath seemed apparent as soon as the initial ECG was recorded.
• An Echo was not done until later. If providers had any doubt about the need for prompt cath after seeing the ECG in Figure-2 — seeing the hypokinetic inferolateral wall motion defect on a bedside Echo could have established a definite need for prompt cath within minutes after seeing the initial ECG.

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Acknowledgment: My appreciation to Ahmed Marai (from Anbar, Iraq) for making me aware of this case and allowing me to use this tracing.

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Me to go back to Blog #337 to see how I described this - OMI criteria !!!!

Me to REDO/UPDATE my Comment in the 7/31/2020 SSmith post !!!!

https://drsmithsecgblog.com/omi-nomi-paradigm-established-as-better/ 

 

 

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.

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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.

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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.

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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).

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

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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.

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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 — The Patient Decided to Leave — EXTRA COPY

The ECG in Figure-1 was obtained from a middle-aged patient — who presented with palpitations. The patient has known ischemic heart disease, and was hemodynamically stable with this rhythm.

QUESTIONS:

• How would you interpret the rhythm in Figure-1?
• Clinically — What would YOU do?

 

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

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

My Initial Thoughts:

I found this rhythm fascinating! The "good news" — is that today's patient was hemodynamically stable with this rhythm — which tells us that we at least have a "moment in time" to contemplate what is going on. 

• As always — I favor the Ps,Qs,3Rs Approach for systematic rhythm interpretation (See ECG Blog #185 for review of the Ps,Qs,3Rs).
• 
  
• HINT #1: It does not matter in what sequence you look for P waves, QRS width, and the 3 Rs of Rate, rhythm Regularity, and whether atrial activity is (or is not) Related to neighboring QRS complexes.
• HINT #2: It sometimes helps to step back a little bit from the tracing when assessing rhythm Regularity.
• HINT #2: Using calipers will be especially helpful for interpreting the rhythm in Figure-1.

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

CHALLENGE: I've labeled today's tracing below in Figure-2 — but before looking at how I labeled this — What do YOU think?

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

Figure-2: I've labeled today's ECG.

Assessing the Ps, Qs, and 3Rs in Today's ECG:

My thoughts in the sequence they came to me were as follows:

• As I did not see upright P waves in front of neighboring QRS complexes — I knew the rhythm was not sinus.
• The QRS is wide (clearly more than half a large box in duration).
• The Rate of this rhythm is not overly fast (ie, with an R-R interval of ~3 large boxes in duration = about 100/minute).
• Although one might initially think the rhythm was regular — stepping back a little bit from the tracing allows us to appreciate that this rhythm is definitely not Regular. Instead — there is a "regular irregularity" — in the form of group beating (Using calipers facilitates recognizing that there are alternating shorter [RED] — then longer [BLUE] R-R intervals). 
• Looking closer at QRS complexes (especially in the inferior leads) — a sharp negative deflection follows each QRS complex in leads II,III,aVF at a fixed distance after each of the 10 beats in this tracing (YELLOW arrows). These negative deflections represent retrograde P waves with a fixed RP' interval ( = 1:1 VA conduction).
• Looking at simultaneously-recorded leads aVR,aVL,V1 — we can appreciate a small, positive pointed deflection that occurs at precisely the same instant in time as these negative deflections. This confirms that these YELLOW arrow negative deflections do in fact represent retrograde P waves (such that these P waves are Related to preceding QRS complexes by a fixed RP' interval — and this rhythm is not AFib).

My Impression of Today's Rhythm: 

To Emphasize: This is an extremely complex rhythm! What follows below goes well Beyond-the-Core!

• At this point in my assessment, given QRS widening with retrograde P waves — I suspected a ventricular rhythm with the unusual finding of group beating.
• The finding of group beating should always suggest the possibility of Wenckebach conduction (See ECG Blog #164 and Blog #457 and Blog #66, among others). It's important to realize that "Wenckebach conduction" is not limited to 2nd-degree AV block of the Mobitz I type. Instead — Wenckebach periodicity can be seen in association with SA block, with AFib, AFlutter and ATach; with retrograde conduction — and on occasion (like today's case appears to be) — with ventricular rhythms! 
• As I schematically show in Figure-3 — what can happen is that there may be a ventricular rhythm that exhibits a form of Wenckebach Exit Block out of the ventricular ectopic focus at the junction of this focus with ventricular myocardium (Credit to Dr. Harry Mond for his explanation of this fascinating and rare phenomenon — Harry's Corner of March 3, 2025).

Figure-3: Schematic of Exit Block from an ectopic ventricular focus.

Laddergram Illustration:

In Figure-4 — I schematically depict what appears to be happening with the Exit Block in today's case. 

• The lower ORANGE-shaded Tier in this laddergram represents events emanating out of the ectopic ventricular focus that I schematically drew in Figure-3.
• As can be seen in the Figure-4 laddergram — because of the Wenckebach Exit Block, only 2 out of every 3 impulses make it out of this ectopic ventricular focus (the Orange-shaded Tier) to arrive at the ventricles.
• 
  
• PEARL #1: If it were not for the Exit Block — the rate of this ectopic ventricular rhythm in today's case would be considerably faster than what it appears to be. We only see 2 out of every 3 ventricular impulses on the surface ECG. The R-R interval within which these 2 ventricular beats occur on the surface ECG equals the distance between beat #1 and beat #3 (which is ~6 large boxes in duration). As a result — the average rate of the ventricular rhythm on the surface ECG (ie, in Figure-4) is ~100/minute.
• But within the ectopic ventricular focus — 3 (not two) impulses are occurring within this R-R interval of ~6 large boxes. Thus, within the ventricular focus — an impulse is formed every 2 large boxes — and 300 ÷ 2 =150/minute. This means that if it were not for the 3:2 Wenckebach Exit Block — that the rate of the ectopic ventricular focus would be a ventricular tachycardia at 150/minute!
• 
  
• Continuing with the laddergram in Figure-4 — Once the 2-out-of-3 ventricular impulses make it out of the ectopic-ventricular junction — they depolarize the ventricular myocardium — and in today's case, also generate 1:1 retrograde conduction back to the atria (YELLOW arrows with a fixed RP' interval after each ventricular beat).

Figure-4: My proposed Laddergram of today's rhythm.

Are there Other Possibilities for Today's Rhythm?

QRS morphology in Figure-2 supports the probability that this represents a ventricular rhythm. That's because:  

• QRS morphology in this tracing does not resemble any of the usual forms of conduction block (ie, Although today's tracing is consistent with LBBB conduction in the limb leads [with an all positive QRS in leads I and aVL] — it manifests a very atypical pattern for either LBBB or RBBB conduction in the chest leads [that show a qR in lead V1, but with tall, positive QRS complexes in each of the remaining 5 chest leads]).

PEARL #2: Rarely — a supraventricular QRS morphology pattern may be seen that resembles LBBB conduction in the limb leads, but RBBB conduction in the chest leads. This pattern is known as MBBB (Masquerading Bundle Branch Block — See ECG Blog #517). 

• With regard to the rhythm in Figure-2 — although I think a ventricular rhythm with Wenckebach Exit Block out of the ventricular focus is the most likely explanation for the regular irregularity that we see in today's tracing — I can not rule out the possibility that this is a junctional rhythm with preexisting MBBB and Wenckebach conduction out of the AV Node.

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

Challenge QUESTIONS: 

We come to the issues of how we might increase the certainty of our rhythm diagnosis? — and the clinical issue of How best to manage today's patient? Consider the following: 

• If you could ask this patient 1 question — What would that question be?
• If there was 1 thing you could get from review of this patient's chart — What would you look for? 

My Answers:

In addition to seeing some basic laboratory results (renal function, serum electrolytes, etc.) and learning whatever else we could about this patient:

• I'd want to know what medication(s) this patient was taking? (ie, To see if any medication might be predisposing the patient  to ventricular arrhythmias).
• I'd want to see a prior ECG on this patient (ie, To see if the unusual QRS morphology seen in Figure-2 was previously present during sinus rhythm).  

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

The CASE Concludes:

Review of this patient's chart revealed that the patient was being seen for psychiatric care — and that he was taking Respiridone.

• It has long been known typical antipsychotic drugs (ie, Chlorpromazine, Haloperidol, Thioridazine, etc.) increase the risk of serious, and even fatal cardiac arrhythmias. It appears that newer atypical antipsychotic drugs (including Respiridone) also significantly increase this risk (Ray et al — N Engl J Med 360(3):225-235, 2009). The mechanism is thought to be the result of blockade of potassium channels with prolongation of cardiac repolarization. Respiridone does prolong the QTc — but by itself, usually not enough to precipitate Torsades de Pointes.
• No previous ECG was found on this patient’s chart (and no indication was seen in the medical chart that the patient previously had arrhythmias).
• The patient was not cooperative — and he signed out against medical advice (It was felt that the patient was sufficiently competent mentally to do so).
• The “good news” — is the fact that this patient felt well enough that he decided to leave suggests that he was not symptomatic with this arrhythmia.
• Unfortunately — no further follow-up is available.

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

Acknowledgment: My appreciation to Cardiology Notes (FB ECG site) for making allowing me to use this case.

• Special acknowledgment also to Omar Hassan Seddik (Mansoura City, Egypt) and Khaled Ash (from Damascus, Syria) for their input and for drawing my attention to this case.

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

 

— OLDER VERSION —

The ECG in Figure-1 was obtained from a middle-aged patient — who presented with palpitations. The patient has known ischemic heart disease, and was hemodynamically stable with this rhythm.

QUESTIONS:

• How would you interpret the rhythm in Figure-1?
• Clinically — What would YOU do?

 

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

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

My Initial Thoughts:

I found this rhythm fascinating! The "good news" — is that today's patient was hemodynamically stable with this rhythm — which tells us that we at least have a "moment in time" to contemplate what is going on. 

• As always — I favor the Ps,Qs,3Rs Approach for systematic rhythm interpretation (See ECG Blog #185 for review of the Ps,Qs,3Rs).
• 
  
• HINT #1: It does not matter in what sequence you look for P waves, QRS width, and the 3 Rs of Rate, rhythm Regularity, and whether atrial activity is (or is not) Related to neighboring QRS complexes.
• HINT #2: It sometimes helps to step back a little bit from the tracing when assessing rhythm Regularity.
• HINT #2: Using calipers will be especially helpful for interpreting the rhythm in Figure-1.

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

CHALLENGE: I've labeled today's tracing below in Figure-2 — but before looking at how I labeled this — What do YOU think?

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

Figure-2: I've labeled today's ECG.

Assessing the Ps, Qs, and 3Rs in Today's ECG:

My thoughts in the sequence they came to me were as follows:

• As I did not see upright P waves in front of neighboring QRS complexes — I knew the rhythm was not sinus.
• The QRS is wide (clearly more than half a large box in duration).
• The Rate of this rhythm is not overly fast (ie, with an R-R interval of ~3 large boxes in duration = about 100/minute).
• Although one might initially think the rhythm was regular — stepping back a little bit from the tracing allows us to appreciate that this rhythm is definitely not Regular. Instead — there is a "regular irregularity" — in the form of group beating (Using calipers facilitates recognizing that there are alternating shorter [RED] — then longer [BLUE] R-R intervals). 
• Looking closer at QRS complexes (especially in the inferior leads) — a sharp negative deflection follows each QRS complex in leads II,III,aVF at a fixed distance after each of the 10 beats in this tracing (YELLOW arrows). These negative deflections represent retrograde P waves with a fixed RP' interval ( = 1:1 VA conduction).
• Looking at simultaneously-recorded leads aVR,aVL,V1 — we can appreciate a small, positive pointed deflection that occurs at precisely the same instant in time as these negative deflections. This confirms that these YELLOW arrow negative deflections do in fact represent retrograde P waves (such that these P waves are Related to preceding QRS complexes by a fixed RP' interval — and this rhythm is not AFib).

My Impression of Today's Rhythm: 

To Emphasize: This is an extremely complex rhythm! What follows below goes well Beyond-the-Core!

• At this point in my assessment, given QRS widening with retrograde P waves — I suspected a ventricular rhythm with the unusual finding of group beating.
• The finding of group beating should always suggest the possibility of Wenckebach conduction (See ECG Blog #164 and Blog #457 and Blog #66, among others). It's important to realize that "Wenckebach conduction" is not limited to 2nd-degree AV block of the Mobitz I type. Instead — Wenckebach periodicity can be seen in association with SA block, with AFib, AFlutter and ATach; with retrograde conduction — and on occasion (like today's case appears to be) — with ventricular rhythms! 
• As I schematically show in Figure-3 — what can happen is that there may be a ventricular rhythm that exhibits a form of Wenckebach Exit Block out of the ventricular ectopic focus at the junction of this focus with ventricular myocardium (Credit to Dr. Harry Mond for his explanation of this fascinating and rare phenomenon — Harry's Corner of March 3, 2025).

Figure-3: Schematic of Exit Block from an ectopic ventricular focus.

Laddergram Illustration:

In Figure-4 — I schematically depict what appears to be happening with the Exit Block in today's case.

• The lower ORANGE-shaded Tier in this laddergram represents events emanating out of the ectopic ventricular focus.
• As can be seen, because of the Wenckebach Exit Block — Only 2 out of every 3 impulses make it out the ectopic ventricular focus to arrive at the ventricles.
• 
  
• PEARL #1: If it were not for the Exit Block — the rate of this ectopic ventricular rhythm would be considerably faster than what it appears to be. We only see 2 out of every 3 ventricular impulses on the surface ECG. The R-R interval within which these 2 ventricular beats occur on the surface ECG equals the distance between beat #1 and beat #3 (which is ~6 large boxes in duration). As a result — the average rate of the ventricular rhythm in Figure-4 is ~100/minute.
• But within the ectopic ventricular focus — 3 impulses are occurring within this R-R interval of ~6 large boxes. Thus, within the ventricular focus 1/3 of the ventricular rate = 300/6 = 50/minute. This means that if it were not for the 3:2 Wenckebach Exit Block — that the rate of the ectopic ventricular focus would be a ventricular tachycardia at 150/minute!
• 
  
• Continuing with the laddergram in Figure-4 — Once the 2-out-of-3 ventricular impulses make it out of the ectopic-ventricular junction — they depolarize the ventricular myocardium — and in today's case, also generate 1:1 retrograde conduction back to the atria (YELLOW arrows with a fixed RP' interval after each ventricular beat).

Figure-4: My proposed Laddergram of today's rhythm.

Are there Other Possibilities for Today's Rhythm?

QRS morphology in Figure-2 supports the probability that this represents a ventricular rhythm. That's because QRS morphology in this tracing does not resemble any of the usual forms of conduction block (ie, Although today's tracing is consistent with LBBB conduction in the limb leads [with an all positive QRS in leads I and aVL] — it manifests a very atypical pattern for either LBBB or RBBB conduction in the chest leads [that show a qR in lead V1, but with tall, positive QRS complexes in each of the remaining 5 chest leads]).
NOTE: Rarely — a QRS morphology pattern may be seen that resembles LBBB conduction in the limb leads, but RBBB conduction in the chest leads. This pattern is known as MBBB (Masquerading Bundle Branch Block — See ECG Blog #517). With regard to the rhythm in Figure-2 — although I think a ventricular rhythm with Wenckebach Exit Block out of the ventricular focus is the most likely explanation for the regular irregularity that we see in today's tracing — I can not rule out the possibility that this is a junctional rhythm with preexisting MBBB and Wenckebach conduction out of the AV Node.

Challenge QUESTIONS:

• If you had 1 question to ask this patient — What would it be?
• If there was 1 thing you could get from this patient's medical records — What would you look for? 

XXXXXX   

Note — rather than "VT" — today's rhythm represents AIVR (AIVR) with Wenckebach conduction out of the ventricular ectopic focus, as the shorter R-R intervals (between the RED arrows) are barely less than 3 large boxes, which correspond to a ventricular rate just over 100/minute (See ECG Blog #108 — for more on distinction between "fast VT" vs AIVR).

Blog 108

https://ecg-interpretation.blogspot.com/2015/04/ecg-blog-108-ventricular-rhythms-aivr-vt.html

Harry Mond LINK 

https://www.cardioscan.co/harrys-corner/an-unusual-ventricular-tachycardia

XXXXXXX

MUST FIX at the END!

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

Acknowledgment: My appreciation to Cardiology Notes (FB ECG site) for making allowing me to use this case.

  — Special acknowledgment also to Omar Hassan Seddik (Mansoura City, Egypt) and Khaled Ash (from Damascus, Syria) for their input and for drawing my attention to this case.

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

 

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

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 !!! )

Greetings Sir — I apologize for texting you late, Yes of course sir, it an honor to me, thank you so much Omar Hassan Seddik, Egypt, Mansoura city.
 
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.