ECG Blog #512 — Important Details ...

The ECG in Figure-1 was obtained from a middle-aged adult — who presented "acutely ill" with septicemia — but no chest pain.

• How would you interpret this ECG?
• Should you activate the cath lab? 
• If not — Why not?

Figure-1: The initial ECG in today's case — obtained from a middle-aged patient with septicemia, but no chest pain. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on this CASE:

The rhythm is sinus, at a rate just under 100/minute (ie, The R-R interval is just over 3 large boxes in duration). Intervals (PR,QRS,QTc) and the axis look normal. No chamber enlargement. 

Regarding Q-R-S-T Changes:

• Q Waves — are seen in each of the inferior leads. At least in lead III — the Q wave looks somewhat wider than is usually seen (which suggests this may be an "infarction Q wave" from an MI that occurred at some point in time).
• R Wave Progression — The R wave in lead V2 looks slightly taller than is generally seen in this lead. That said, the point for transition (ie, where the R wave becomes taller than the S wave is deep) — is normal (seen here to occur between lead V2-to-V3).

Regarding ST-T Wave Changes: 

• The 3 inferior leads (seen in Figure-2 within the RED rectangles) — each show slight-but-real ST elevation, with ST segment straightening in leads II and III.
• PEARL #1: Viewed in isolation — it would be difficult to know if the Q waves and slight-but-real ST elevation that we see in leads II,III,aVF indicate an acute (or recent) OMI, especially given the absence of CP (Chest Pain). But in the context of lead aVL (that manifests a nearly perfect, mirror-image opposite picture to what we see in lead III) — we have to at least consider a recent or acute event until proven otherwise (Note the slight ST depression with terminal T wave positivity seen within the BLUE rectangle in Figure-2). 
• KEY Point: As shown in ECG Blog #171 — Blog #158 and Blog #474 (among others) — one of the most helpful clues for determining whether subtle ST elevation in the inferior leads represents acute or recent OMI — is the presence of a mirror-image opposite ST-T wave picture between leads III and aVL. I find this reciprocal relationship almost "magical" in its reliability for suggesting an acute OMI (Occlusion-based Myocardial Infarction) based on the nearly opposite anatomical location in the frontal plane of lead III (at +120 degrees) and lead aVL (at -30 degrees). 

Figure-2: I've labeled key findings in the initial ECG.

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

• NOTE #1: See my ADDENDUM below for review of the concept of what is an "OMI" (vs the outdated concept by clinicians "stuck" on insisting on STEMI criteria before they consider thrombolytic therapy or cath with PCI).
• NOTE #2: In today's case — Assessment as to whether STEMI criteria are met is difficult (ie, Seeing whether ≥1 mm of ST elevation is attained in at least 2 inferior leads). This is because there is PR segment depression in the inferior leads in Figure-2. Clinically, this should not matter — because what really counts is whether or not there is acute coronary occlusion — and PEARLS #1 and 2 suggest that an OMI is present regardless of whether or not STEMI criteria are satisfied!

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

PEARL #2: Additional support regarding our concern for an ongoing acute inferior OMI — is forthcoming from the appearance of lead V2 (BLUE arrow in this lead in Figure-2).

• Because of the common blood supply in most patients between the inferior and posterior walls of the left ventricle — seeing a suggestion of acute posterior OMI adds support that uncertain limb lead findings are likely to be "real".
• This is precisely what we see in Figure-2. As is often emphasized in this ECG Blog — there normally is slight, upward sloping ST elevation in leads V2 and V3. However, the BLUE arrow in lead V2 highlights ST-T wave flattening with slight ST depression in this lead that is clearly abnormal.
• KEY Point: When inferior OMI is suspected — the presence of ST depression that is maximal in leads V2, V3 and/or V4 suggests associated posterior OMI. And, in today's case — it is this ST-T wave flattening and depression in lead V2 that tells us we have to consider the inferior lead ST elevation as recent until proven otherwise.
• 
  
• PEARL #3: In addition to suspected recent infero-postero OMI — there may also be RV involvement in Figure-2. This is because, rather than ST depression — the ST segment in lead V1 is coved and not at all depressed (as would be expected with a posterior OMI). 
• If there is simultaneous posterior OMI and acute RV involvement — then ST elevation in right-sided lead V1 from the RV MI may attenuate the amount of ST depression that we would otherwise see in lead V1 from posterior OMI. For this reason — an ECG with right-sided chest leads would ideally have been recorded as the best way to quickly determine if there is (or is not) RV involvement (See ECG Blog #190 for more on ECG recognition and management concerns regarding acute RV involvement).
• 
  
• PEARL #4: More than the ST-T wave flattening and depression that we see in lead V2 — the remaining leads in Figure-2 are also abnormal (ie, leads I; V3,V4,V5,V6 all manifest either ST-T wave flattening and/or a lack of clearly upright T waves). In the context of suspected recent or acute infero-postero OMI — these nonspecific ST-T wave findings suggest that in addition to the acute event, the patient may have significant underlying multi-vessel disease.

MY Clinical Impression: This is a difficult case — that is clearly complicated by the following: i) This patient is acutely ill with septicemia; — and, ii) The patient is not having chest pain! That said — my thoughts when this case was sent to me were the following:

• There most likely has been a recent infero-postero OMI. Whether this represents an ongoing acute event is impossible to determine from this single ECG without the benefit of additional clinical information (ie, a more complete history; comparison with a previous "baseline" ECG to see if the above-described ECG changes are "new"; serial Troponins; Echo at the bedside looking for a localized wall motion abnormality; etc.).
• Right-sided chest leads would have ideally been obtained to assess for the possibility of associated RV MI.
• Apart from any acute event — this patient may have multi-vessel disease with an unknown pattern of collateralization.
• Cardiac catheterization (sooner rather than later) may be needed to determine if an acute event is ongoing. That said — the timing for when to perform cardiac cath is complicated by the patient's other acute illness ( = septicemia). Ideally, at least some degree of stabilization would be achieved before beginning to contemplate acute intervention from this patient's presumed OMI. Admittedly — determining the optimal moment for intervention is a "juggling" act.

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

The CASE Continues:

• The patient responded positively to initial treatment of his septicemia.
• Additional history was obtained — indicating that the patient did have chest pain prior to coming to the hospital!
• Initial Troponin was moderately elevated.
• As shown in Figure-3 — a repeat ECG was obtained. The patient's CP was "less" at the time of this repeat ECG.

QUESTIONS regarding Figure-3:

• How would you interpret the repeat ECG?
• Does Figure-3 confirm the diagnosis of an acute OMI?

Figure-3: Comparison between the 2 ECGs in today's case.

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

MY Answers:

Clinically, the most useful way to interpret the repeat ECG shown at the bottom in Figure-3 — is to compare this tracing with today's initial ECG.

• First — Note how much easier it is compare serial ECGs when the 2 tracings you are looking at are placed side-by-side (as they are in Figure-3).
• My overall impression — is that the repeat ECG is clearly improved compared to the initial ECG that appears at the top of Figure-3.
• Of note — QRS amplitude is reduced in many leads in the repeat ECG. This is of uncertain significance. However, the frontal plane axis and R wave progression in the chest leads are similar in both tracings — such that lead-by-lead comparison should be valid.
• Accounting for the reduced QRS amplitude in ECG #2 — ST elevation is less in each of the inferior leads, and the reciprocal ST depression that had been seen in lead aVL (and to a lesser extent in lead I) on the initial ECG is no longer present. 
• In the chest leads — ST coving in lead V1 is less. 
• ST depression is no longer seen in lead V2, now with some return of a T wave in this lead.
• Lateral chest lead ST-T waves now look less abnormal.

BOTTOM Line:  The moderately elevated Troponin confirms infarction. Given reduction in the severity of this patient's CP in association with the above subtle-but-real improvement in ST-T wave appearance — I interpreted the repeat ECG in Figure-3 as suggestive of "dynamic" ST-T wave changes, providing further support of an evolving acute event.

• Cardiac catheterization was performed — and revealed severe triple-vessel disease!
• Unfortunately, I lack further details regarding follow-up.

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

Final PEARL:

Figuring out what happened when with respect to acute coronary occlusion is challenging at best — and nearly impossible to do in the absence of timely documentation during the process.

• In my experience — correlation between the presence and relative severity of CP and the timing of each ECG obtained — can rarely be determined by retrospective review of the patient's chart.
• That said — Wouldn't it be EASY to document this correlation between CP severity with each serial ECG if this was done at the time that the patient is being evaluated in the ED? (ie, Medical providers can simply write ON each actual ECG [as well as in the chart] the severity of CP at the time each ECG is recorded).
• Doing so would then give us a "story" — that we can then piece together into the most reasonable clinical scenario (that should tell us if the "culprit" vessel is open or closed at the time of each tracing).
• Doing so would also clue us into the "pseudo-normalization" period that may occur following spontaneous reperfusion with reduction in CP (ie, No more than minimal if any ECG abnormalities may be seen if the initial tracing occurs in between the period of ST elevation on the way to reperfusion T wave inversion).
• For example, in today's case — knowing that the patient's CP had decreased in association with the timing of the repeat ECG allowed us to appreciate that relatively modest improvements in ECG findings are consistent with "dynamic" ST-T wave changes.

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

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

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

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

ADDENDUM (1/3/2026): 

For more regarding the concept and ECG interpretation of OMIs (that do not satisfy millimeter-based STEMI criteria):

• Check out ECG Blog #337 — that reviews a case with focus on distinction between a "NSTEMI" vs an OMI.
• Consider the 2 Audio Pearls at the bottom of this page.
• Consider Figure-4 — which reviews some ECG findings to look for when you suspect an acute OMI in a patient who does not satisfy the millimeter-based STEMI criteria that I review below this Figure.

Figure-4: ECG findings to look for when your patient with new-onset cardiac symptoms does not manifest STEMI-criteria ST elevation on ECG.
= = = = =
KEY Note #1: Insistence in satisfying millimeter-based STEMI criteria before considering prompt cath with PCI (or thrombolytic therapy when access to 24/7 cath-capability is not available) — will miss at least 1/3 of all acute coronary occlusions. In a patient with new CP — attention to the ECG findings in Figure-4 may allow you to identify these patients with an acute OMI despite lacking STEMI criteria.
= = = = =
KEY Note #2: Loss of potentially viable myocardium is actually much greater than that implied in Note #1 — because even for patients in whom a "STEMI" is eventually recognized — by waiting until millimeter-based criteria are finally satisfied, the needed reperfusion therapy (PCI or thrombolytic therapy) is all-too-often delayed (often by many hours!). Time is critical! — as the greatest amount of potential myocardial-saving benefit occurs when reperfusion therapy is provided within the first few hours! (with the self-fulfilling prophecy that the outdated and inferior "STEMI-paradigm" gets perpetuated in the literature — because data will be recorded saying PCI was delivered "within minutes" of STEMI elevation [neglecting the clinical reality that OMI-criteria will often have been present hours earlier! ] ).
= = = = =
Note #3: See ECG Blog #318 — for clarification of T-QRS-D (Terminal QRS Distortion = my 2nd bullet in Figure-4).

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

How a "STEMI" is Defined:

I've excerpted the following Akbar and Mountfort's citation in StatPearls, 2024 — of ECG Guidelines for defining a "STEMI" from the AHA (American Heart Association), ACC (American College of Cardiology), ESC (European Society of Cardiology), and the WHF (World Heart Federation):

• New ST-segment elevation of ≥1 mm at the J point in 2 contiguous leads (except in leads V2 and V3).
• 
  
• In leads V2 and V3:
• ST elevation ≥2 mm for men >40 years of age.
• ST elevation ≥2.5 for men ≤40 years of age.
• ST elevation ≥1.5 mm for women.

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

—  —

ECG Media PEARL #10 (10 minutes Audio) — reviews the concept of why the term “OMI” ( = Occlusion-based MI) should replace the more familiar term STEMI — and, reviews the basics on how to predict the "culprit" artery.

—  —

ECG Media PEARL #11 (6 minutes Audio) — Reviews how to tell IF the “culprit” (ie, acutely occluded) artery has reperfused, using clinical and ECG criteria.

 

ECG Blog #511 — A Patient with Chest Pain ...

The ECG in Figure-1 was obtained from an older man who presented to the ED (Emergency Department) for new CP (Chest Pain).

• Thinking the rhythm is VFib (Ventricular Fibrillation) — the emergency team went to charge the defibrillator.

QUESTIONS:

• Do YOU agree?
• How certain are you about what to do?

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

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

ANSWER:

The rhythm in Figure-1 should not be shocked. 

• I was sent this case — and immediately responded with 100% certainty that the rhythm is not VFib.
• The 1st thing to do is to go to the bedside to Check the patient! Although possible to maintain consciousness for a period of seconds at the onset of VFib — If your patient is alert and talking, then you have confirmed this is not VFib.
• Check the Left Leg extremity. This is almost certain to be the principal source of the Artifact that we see in Figure-1 (ie, from a faulty LL electrode connection? — or from excessive tremor in the left leg?).
• Repeat the ECG. Since this older man presented to the ED for new CP — We want to obtain a technically adequate 12-lead ECG to ensure that there is no sign of an acute cardiac event.
• Stay at the bedside while the repeat ECG is recorded. If the same artifact distortion appears while the repeat ECG is recorded — you want to be there to problem solve the source of the artifact.

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

How Do We Immediately Know this is Artifact?

If we simply looked at the 5 limb leads beginning with lead II — it would be easy to think this patient had just gone into VFib. However, the presence of a regular rhythm for the 5 simultaneously-recorded beats in lead I immediately tells us that the rhythm is not VFib.

• Artifact is common. Potential sources of artifact include tremor, shivering, brief seizure activity or other body movement; loose or faulty lead connection; external devices that may produce various types of interference; and application of a monitoring lead in close contact with a pulsating artery, among others. 
• The clinical reality — is that recording an ECG on an acutely ill patient may sometimes result in unavoidable artifact. That said — a general interpretation of the ECG will usually still be possible despite a technically imperfect recording. The BEST way to prove artifact — is to recognize persistence of an underlying spontaneous rhythm that is unaffected by any erratic or suspicious deflections that are seen (as is shown in Figure-2). 

Figure-2: I've labeled today's tracing to prove this is not VFib.

This is Not VFib:

The BLUE arrows in Figure-2 prove that the rhythm is not VFib.

• Baseline artifact is seen in lead I. That said, even though we cannot be certain if there is (or is not) atrial activity in this lead — we can easily recognize that a regular rhythm with 5 fairly normal-appearing narrow QRS complexes is present.
• The BLUE arrows that I've drawn under beat #2 — show that QRS complexes can also be seen to occer at the same moment in time in other leads. This is most easily appreciated in lead aVL — in which we can recognize 5 regular QRS complexes occurring simulaneously with the 5 regular beats that we see in lead I.
• Specifically in lead aVL — the 3rd QRS complex is the most difficult to recognize, because it is preceded by high-amplitude artifact deflections. But the 1st, 2nd, 4th and 5th QRS complexes in lead aVL are clearly evident.
• 
  
• KEY Point: What makes it especially challenging to appreciate artifact in today's tracing — is the presence of baseline artifact undulations in each of the limb leads, even in lead I. But 5 regular QRS complexes are seen not only in lead I — but also in all 6 chest leads that display these same 5 supraventricular beats. Presumably this is a normal sinus rhythm at ~60/minute, albeit there is too much baseline artifact to make out P waves.

Identifying the "Culprit" Lead:

Einthoven's Triangle tells us to immediately look at the patient's Left Leg for the source of artifact. Note the following:

• The relative amount of artifact distortion is approximately equal in 2 of the 3 standard limb leads (ie, leads II and III) — but is minimal in the 3rd limb lead (ie, other than the small amplitude baseline artifact in lead I — the high amplitude artifact deflections are not seen).
• By Einthoven’s Triangle (See Figure-3 below) — the finding of equal artifact distortion in Lead II and Lead III, localizes the “culprit” extremity to the LL ( = Left Leg) electrode.
• The absence of these high-amplitude artifact deflections 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 the Audio Pearl below — the finding of maximal amplitude artifact in unipolar lead aVF confirms that the left leg 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.

Figure-3: Using Einthoven's Triangle to identify the "culprit" extremity.

CASE Follow-Up:

Although providers brought the defibrillator to the bedside — they found the patient to be alert and oriented. The ECG monitor on the defibrillator showed sinus rhythm without artifact — at which point providers realized the problem was a loose electrode.

• After fixing the loose connection — a normal ECG was recorded.

CHALLENGE:

Take a LOOK at ECG Blog #490.

• Can you identify the problem? (The Answer on Blog #490).

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

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

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

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

ADDENDUM (12/27/2025):

• 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.

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

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 above in today's case.

• 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-2; — 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.
• Similarly — the amplitude of the artifact deflections in the 6 unipolar chest leads that we saw in Figure-2 — is also significantly reduced from the maximal amplitude seen in leads II, III and aVF.

  

BOTTOM LINE: Artifact is common in real-life practice. With a little practice, you can immediately know that the bizarre deflections you see are the result of artifact — and, when a single extremity is responsible, you can identify within seconds the "culprit" extremity.

• Nothing else shows the relative amount of artifact in the mathematical relationships described above, in which there is equal maximal artifact deflection in 2 of the 3 limb leads (with the 3rd limb lead being spared) — and 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 in today's case is lead aVF — which is a unipolar lead recorded from the left leg).

 

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). 

ECG Blog #510 — Myocarditis or Acute MI?

You are shown the ECG in Figure-1 — obtained from a young adult with palpitations. Is the ST elevation in the chest leads the result of:

• an acute MI? 
• or myocarditis? 
• or is it a normal repolarization variant?

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

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

About the ST Elevation …

• For clarity in Figure-2 — RED dotted lines in leads V2-thru-V6 highlight the baseline for assessing chest lead ST elevation in this tracing.
• RED arrows highlight the J-point in leads V4,V5,V6 — which serves as the landmark for judging the amount of ST elevation.

QUESTIONS regarding Figure-2:

• Did YOU begin your interpretation of today’s initial ECG by assessing the rhythm?
• HINT: Why is it especially important to begin by assessing the rhythm in today’s tracing?

Figure-2: I’ve labeled the J-point in leads V4,V5,V6 — which serves as the baseline for judging the amount of ST elevation. 

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

ANSWER:

The reason it’s important to first assess the rhythm in the long lead II (at the bottom of today’s tracing) — is that the shape of the P waves is not always the same, and the amount of ST elevation in this ECG varies depending on the shape of the P wave that precedes each beat.

• PEARL #1: Today’s case provides a prime example for why it is important to begin interpretation of every ECG you encounter — by spending an educated 2-3 seconds looking in front of each QRS complex to see if there is a P wave. 
• If so — Is the shape of each P wave the same? 
• Is the PR interval constant?

Depending on how your ECG machine is set up — one or more long lead rhythm strips may be displayed under the 12-lead ECG. 

• I favor systems that display a long lead II (instead of a lead V1 or other lead) — because IF upright P waves are present in lead II with a constant PR interval in front of each QRS complex — then a normal sinus rhythm is present (This is not necessarily true if a lead other than lead II is used for recording the long lead rhythm strip).

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

Take another LOOK at the long lead II rhythm strip in Figure-2.

• QUESTION: Is sinus rhythm present in this tracing?

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

ANSWER:

Upright P waves with a constant PR interval are present for only 3 beats in today’s tracing. As shown in Figure-3 — only beats #6,7,8 are sinus-conducted (RED arrows), albeit with a variable R-R interval.

Figure-3: RED arrows highlight the 3 sinus P waves in today’s tracing.

QUESTION:

• How many P wave shapes are there in Figure-3?
• Clinically — What does this mean?

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

ANSWER:

There are at least 3 (if not 4) P wave shapes in today’s tracing. We show the most commonly occurring shape in Figure-4.

• YELLOW arrows in the long lead II highlight a run of 6 beats in a row that are preceded by large negative P waves, which have a short but constant PR interval ( = beats #10-thru-15). The R-R interval for these 6 beats is fairly constant — at a rate just under 100/minute. This suggests that these 6 beats represent an accelerated junctional focus.
• The other (less common) possibility for this 6-beat run of QRS complexes preceded by negative P waves of this size — is that beats #10-thru-15 could represent a low atrial focus.

Figure-4: Large size, YELLOW arrow P waves with a short but constant PR interval precede beats #10-thru-15.

For simplicity in Figure-4 — Let's assume that all of the YELLOW arrow P waves arise from the same accelerated junctional focus.

• We then have to explain why there are other P wave shapes in front of the remaining beats on this tracing. 
• Note that the rhythm in Figure-4 begins with a similar large-sized negative P wave ( = the first YELLOW arrow in Figure-4).

QUESTION:

I highlight the different P wave shapes in the long lead II rhythm strip with additional colored arrows in Figure-5.

• Can you explain the mechanism of today's rhythm?

Figure-5: Colored arrows highlight the different P wave shapes.

MY Thoughts on Today's Rhythm:

More than a single explanation may be possible for the unusual sequence of P wave shapes in Figure-5.

• I find it easiest to begin by looking at the 3 sinus-conducted beats ( = the 3 RED arrow P waves that highlight the upright P waves preceding beats #6,7,8 in Figure-5).
• Note that the PINK arrow P wave that precedes beat #9 manifests an intermediate P wave shape between the 3 larger upright P waves that precede sinus-conducted beats #6,7,8 — and the 6 consecutive negative P waves that precede beats #10-thru-15. 
• I suspect the reason for this intermediate P wave shape — is that the PINK arrow P wave preceding beat #9 represents an atrial fusion beat that occurs as the underlying sinus rhythm is being overtaken by the accelerated junctional rhythm that emerges with beat #10.
• Note that the rhythm in Figure-5 begins with a single junctional beat (highlighted by the YELLOW arrow that precedes beat #1).
• I'm uncertain if the 4 BLUE arrow P waves that follow in beats #2,3,4,5 represent the emergence of another atrial focus (as might be seen with a wandering atrial pacemaker) — or more likely represent additional atrial fusion beats until the slightly early-occurring sinus beat #6 briefly takes over — before being usurped by the accelerated junctional rhythm beginning with beats #9,10.

Putting It All Together:

Clincally — the details for what each differently-shaped P wave represents are less important than the overall impression of what appears to be happening.

• Today's patient is a young adult who presented for palpitations.
• The underlying rhythm appears to be sinus (beats #6,7,8).
• This sinus rhythm appears to be intermittently usurped by an accelerated junctional rhythm.
• While impossible from this single tracing to rule out interaction with a wandering atrial pacemaker — I think this is less likely than there being a series of atrial fusion beats, as control of the rhythm shifts back-and-forth between sinus beats and the accelerated junctional focus (The change in P wave morphology that is typically seen with a wandering pacemaker tends to be much more gradual than what we see here).
• PEARL #2: The reality is that accelerated junctional rhythms are not commonly seen in adults. Therefore, evaluation of this patient should consist of determing IF one or more underlying precipitating factors are present (ie, assessment of serum electrolytes, blood count, thyroid function studies, and Echocardiogram to rule out structural abnormality — as well as a careful history to rule out alcohol and/or ingestion of recreational substances that might precipitate the accelerated usurping rhythm).
• If this rhythm persisted despite a negative evaluation that fails to reveal a precipitating cause — then empiric treatment with a ß-blocker might be the simplest and most effective approach. (Unfortunately, I don't have follow-up as to the management approach selected for this patient).

============================== 

But what about the ST elevation that we saw in Figure-2?

• I highlight this ST elevation in Figure-6 — with dotted RED lines in those leads in which we see ST elevation.

QUESTION:

• Is there any relation between P wave shape — and whether the QRS complex that follows will manifest an elevated ST segment?

Figure-6: Dotted RED lines highlight which leads manifest ST elevation. Is this related to the preceding P wave shape?

ANSWER:

Today's case represents a unique illustration of the Emery Phenomenon — in which the oppositely-directed atrial repolarization wave (ie, the T of the P wave) produces a "pseudo"-ST elevation effect because of the relatively large size of the negative inferior lead P waves, with short PR interval (See ECG Blog #308).

• Most of the time — the Tp (also known as the "Ta" or atrial T wave) is hidden within the QRS complex. But on those uncommon occasions when a large negative P wave with short PR interval is seen — the resultant oppositely-directed Tp may simulate acute infarction (See My Comment in the June 3, 2020 post in Dr. Steve Smith's ECG Blog for discussion of the Emery Phenomenon in the context of a case that went to cath because of this "pseudo"-ST elevation).

To illustrate this phenomenon — I’ve adapted Figure-7, which I’ve taken from a 2015 post on the Arnel Carmona's ECG Rhythms website.

• As suggested in Figure-7 — the atrial repolarization wave (ie, the T of the P wave) is always present — but with sinus rhythm, the timing of the Tp will largely coincide with the timing of the QRS complex, and therefore not be noticed on the ECG (dotted RED half circle, seen to the left in Figure-7).
• As shown in Figure-7 — the Tp will be oppositely directed to the P wave. Therefore, with normal sinus rhythm (in which by definition, the P wave will be upright in lead II) — the TP will be negative in inferior leads.
• IF the P wave in lead II is negative (as may occur with either a low atrial or junctional rhythm) — then the Tp will be upright (dotted RED half circle, seen to the right in Figure-7). If the Tp wave is large in size and upright — it may distort the end of the QRS complex, and produce the false impression of ST elevation.

Figure-7: Illustration of the Emery Phenomenon. (I have adapted this Figure from the 2015 post by Dr. Bojana Uzelac on Arnel Carmona’s ECG Rhythms website).

KEY Points:

• The size of the Tp wave will be proportional to the size of its P wave. A small P wave will produce a correspondingly small Tp wave. A large P wave will produce a much bigger Tp wave.
• Actually, the effect of the oppositely-directed atrial repolarization wave ( = the Tp — also known as the "Ta" or atrial T wave) will be even larger than shown above in Figure-7 — because normal duration of the Ta wave is significantly longer (up to 2-3 times longer) than normal P wave duration (Francis). This may account for an exaggerated effect on the ST segment when the P wave is large.
• That said — I preserved the same relative proportions in Figure-7 as were seen in the original version of this Figure taken from the ECG Rhythms website. Note that the PR interval for the negative P wave in Figure-7 is almost as long as the PR interval for normal sinus rhythm. But IF the PR interval for the negative P wave is shorter (as occurs in today’s case) — then the upright Tp wave that will be seen with a junctional rhythm will be further displaced to the right, which will produce a much greater degree of pseudo-ST-elevation!

PEARL #3: The fascinating aspect of today's rhythm is that we can see this effect that the changing P wave morphology has — on the amount of ST elevation in the QRS that follows!

• Go BACK to Figure-6. Note that the amount of ST elevation is greatest for QRS complexes that follow negative P waves (ie, for the ST segments of beats #1; and #10-thru-15).
• In contrast — there is no ST elevation following sinus beats #6,7,8.
• 
  
• KEY Point: Awareness that of the Emery Phenomenon in today's case is responsible for pseudo-ST-elevation allows us to discard concern about myocarditis or acute ischemia — and focus our management on treating this patient's palpitations caused by the intermittent usurping accelerated junctional rhythm! There is no real ST elevation in today's case.

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

Acknowledgment: My appreciation to Rasheed Tamimi (from Yemen, Sana'a) for the case and this tracing.

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

Additional Relevant Material to Today's Case:

• See ECG Blog #185 — for review of the Systematic Ps, Qs, 3R Approach to rhythm interpretation.
• See ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
• 
  
• For more on distinction between Low Atrial vs Junctional rhythm — Please see My Comment at the bottom of the page in the January 28, 2019 post in Dr. Smith's ECG Blog.
• 
  
• See ECG Blog #290 and ECG Blog #308 — for more examples of the Emery Phenomenon.
• And for additional cases of the Emery Phenomenon — Please see My Comment at the BOTTOM of the page in the June 3, 2020 post and in the February 23, 2023 post in Dr. Smith's ECG Blog.