ECG Blog #255 (18) — Why AV Dissociation?

The ECG shown in Figure-1 was obtained from a young adult who presented with a presyncopal episode. 

• What is the cause of the AV dissociation?

Figure-1: ECG from a young adult who presented with a presyncopal episode.

  

My Initial Thoughts on Seeing this Tracing:

When I first saw this ECG — my "eye" was immediately drawn to the deflections that I highlight with BLUE arrows in Figure-1. I initially thought this tracing had to represent some unusual form of AV dissociation.

• CONFESSION: This is a trick tracing! I fully acknowledge that I deliberately chose this tracing to illustrate how easy it is to be fooled by artifact. My goal for this post is to review some of the ways to rapidly recognize when artifact is present — since this is usually not taught "in the textbook".

 

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NOTE: Some readers may prefer at this point to listen to the 7:45-minute ECG Audio PEARL before reading My Thoughts regarding the ECG in Figure-1. Feel free at any time to refer to My Thoughts on this tracing (that appear below ECG MP-18).

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Today’s ECG Media PEARL #18 (7:45 minutes Audio) — Reviews recognition of Artifact — and — using Einthoven's Triangle to determine within seconds the "culprit" extremity causing the Artifact on your ECG (This Audio Pearl was first published in ECG Blog #201. That blog post illustrates a case in which artifact is initially mistaken for acute ST elevation).

 

HOW Did I Know there was Artifact in Figure-1?

There are several clues that strongly suggest the BLUE arrow deflections in Figure-1 are not P waves at all — but instead, are pointing to artifact. These clues include:

• The shape of these deflections is geometric. That is — these deflections in each of the inferior leads are much taller than is usually seen for P wave amplitude. These deflections consist of a very steep and straight upward line that ends in a point. It is distinctly unusual to see a physiologic P wave with such a sharp point despite having such a narrow base. Elsewhere, in leads aVR and aVL — these deflections appear as a short, negative skinny line. Physiologic P waves virtually always have at least some width (and should not appear as a very thin, vertical line). This "geometric" appearance of these deflections looks like artifact (and when unusual-looking deflections "look like" artifact — this is because they usually are artifact).
• As suggested by the BLUE arrows in the long lead II rhythm strip — the distribution of these deflections does not make physiologic sense. It is possible for atrial and junctional rhythms to be dissociated with nearly equal rates. This occurs with isorhythmic AV dissociation (See ECG Blog #195), in which P waves and junctional QRS complexes may move with respect to each other's position, but still appear close to each other throughout the duration of the rhythm strip. In contrast, in Figure-1 — the BLUE-arrow deflections appear in all phases of the R-R interval. And while it is possible for there to be complete AV block — this usually does not occur with both atrial and junctional rates being as fast as they are in Figure-1.
• Underlying sinus P waves are regularly seen in several of the leads in Figure-1. The BEST clue for recognizing artifact — is being able to identify the underlying original rhythm that continues unaffected by the deflections you suspect are artifact. These regularly-occurring normal P waves are best seen in lead I of Figure-1.
• The relative size of the deflections in Figure-1 that are suspected of being artifact manifest the precise relative dimensions expected when artifact is caused by a "culprit" extremity (as shown within the colored circles in Figure-2).

Figure-2: I've added colored circles that enclose artifact spikes in each of the leads of today's ECG. Maximal artifact deflections are encircled by BLUE — smaller deflections by RED — and the smallest deflections by YELLOW (See text).

PEARL #1: The relative size and distribution of artifact deflections in Figure-2 precisely follow the location and relative amount of amplitude distortion predicted by Einthoven’s Triangle. By this I mean:

• The height of the artifact spike is approximately equal in 2 of the limb leads (ie, in leads II and III) — and, not seen at all in the 3rd limb lead (ie, no artifact at all is seen in lead I). By Einthoven’s Triangle (See the above picture posted with today’s ECG Media Pearl — which shows Einthoven’s Triangle in the righthand corner) — the finding of equal artifact amplitude 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 MP-18 Audio Pearl above — the finding of maximal amplitude artifact in unipolar lead aVF confirms that the Left Leg is the “culprit” extremity.

 

  

NOTE: I reproduce below in Figures 5, 6 and 7 — 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 arising from a single extremity. These principles are illustrated in Figure-2:

• 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 (contained within the BLUE circle); 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 (contained within the RED circles in Figure-2).
• Similarly — the amplitude of the artifact deflections in the 6 unipolar chest leads in Figure-2 is also significantly reduced from the maximal amplitude seen in leads II, III and aVF (contained within the YELLOW circles in Figure-2).

 

PEARL #2: As alluded to earlier, the BEST clue for confirming that suspicious deflections are truly the result of artifact — is IF you are able to identify the underlying original rhythm that continues unaffected by the deflections you suspect are artifact.

• RED arrows in Figure-3 clearly show continuation of the underlying regular sinus rhythm. This is easiest to see in lead I — because no artifact is seen in this lead. From the 3 sinus P waves in lead I — it can be seen that a regular P-P interval continues for the 4 on-time sinus P waves that are then seen after the lead change in lead aVR (RED arrows in lead aVR).
• Vertical PURPLE lines in the long lead II rhythm strip highlight regularly-occurring sinus P waves that are unrelated to the BLUE-arrow artifact deflections. This proves these deflections represent artifact.

Figure-3: I've added RED arrows to several leads to show continuation of regularly-occurring sinus P waves. In the long lead II rhythm strip — I've added vertical PURPLE lines over regularly-occurring sinus P waves that continue despite the BLUE-arrow artifact deflections (See text).

 

PEARL #3: The goals of identifying the source and cause of artifact are: i) To avoid erroneous interpretation of the ECG (For example, there is no AV dissociation in today's case!); and, ii) To hopefully fix the cause of the artifact so that a better quality tracing can be obtained.

• The above deductive process identifies the source of the artifact in today's tracing as coming from the Left Leg. 
• The fact that the artifact in today's case is completely unrelated to the QRS complex (ie, BLUE arrows in Figure-3 occur at all points in the cardiac cycle) — rules out causes related to cardiac contraction (such as contact of a lead electrode with a pulsating artery).
• Clinically — Now that we know that the artifact arises from something occurring in the patient's left leg — the BEST way to determine the cause of this artifact would be to GO to the bedside and LOOK at the patient (with special attention paid to the patient's left leg, in the hope of identifying the cause of the repetitive artifact activity).

 

FOLLOW-UP to Today's Case: For clarity — I've added a 2nd ECG done the same day on today's patient (Figure-4).

• Similar small-amplitude sinus P waves with the same slightly shortened PR interval are seen in ECG #2, as were seen in the initial ECG #1. But note that there is no longer any artifact seen in ECG #2 (ie, in the bottom tracing in Figure-4).
• The fact that P wave morphology in ECG #2 is identical to those sinus P waves that we were able to see in ECG #1 (RED arrows in the initial ECG) — provides additional confirmation that the geometric-looking deflections (highlighted by BLUE arrows in ECG #1) were in fact the result of some kind of artifact arising from the patient's left foot.
•  
• P.S. — You may have noticed (and been impressed by) the marked increase in QRS amplitude and anterior lead ST-T wave changes seen in both ECG #1 and ECG #2. These tracing were obtained from the same patient I presented in my previous ECG Blog #254. As discussed in the conclusion to that case — these ECG findings did not represent Wellens' Syndrome, nor HCM (Hypertrophic CardioMyopathy), nor LVH — but instead, by exclusion — were felt to represent a repolarization variant.

Figure-4: I've added a 2nd ECG done the same day on this patient (See text).

 

 

BOTTOM LINE: You will see artifact frequently in your real-life clinical work. With a little practice, you can get good at rapidly recognizing that unusual deflections (such as those seen in today's case) — are the result of some form of artifact.

• Nothing else shows 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 with maximal artifact (according to Einthoven’s Triangle).
• Determining if artifact deflections manifest a fixed relationship to the QRS complex (as was seen in ECG Blog #201) — vs being totally unrelated to neighboring QRS complexes (as was the case in today's tracing) — will instantly tell you IF artifact deflections are related to cardiac contraction (or arterial pulsations) — or — IF artifact is related to some local causative factor.

 

Figure-5: Page 475 from the Rowlands and Moore article referenced above (See text).

 

Figure-6: Page 476 from the Rowlands and Moore article referenced above (See text).

 

Figure-7: Page 477 from the Rowlands and Moore article referenced above (See text).

 

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Acknowledgment: My appreciation to Ghady Rahhal (from Virginia, USA) for the case and this tracing.

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Additional Relevant ECG Blog Posts to Today’s Case:

• ECG Blog #201 — Reviews a case of Artifact due to arterial pulsations (with derivation of the "culprit" extremity). 
• ECG Blog #195 — Reviews the phenomenon known as isorhythmic AV Dissociation (in which the atrial and junctional [or ventricular] rate is virtually equal, but P waves are not conducting to the ventricles).

 

Regarding ECG Recognition of ARTIFACT: 

• ECG Blog #148 — Artifact simulating VFib. 
• ECG Blog #44 — Artifact produced by Parkinsonian tremor 
• ECG Blog #139 — Artifact simulating AFlutter. 
• ECG Blog #132 — More artifact simulating VT-VFib. 
• 
  
• Brief review by Tom Bouthillet on some common causes of artifact.

 

Finally — I link to several illustrative Cases taken from Dr. Smith’s ECG Blog. For each of these posts — Please scroll down to the bottom of the page to see My Comment. These cases provide insight to assessment for ARTIFACT:

• The September 27, 2019 post in Dr. Smith’s ECG Blog — for an example of how to recognize the source of extremity artifact. 
• The October 17, 2020 post in Dr. Smith’s ECG Blog — for an example of VT-like artifact
• The January 30, 2018 post in Dr. Smith’s ECG Blog — for arterial pulsation artifact (Please click on the COMMENTS to this post to see my discussion).

ECG Blog #254 (26a) — Wellens Syndrome?

The ECG in Figure-1 was obtained from a 30-ish year old man with a history of a bicuspid aortic valve. He presented to the ED (Emergency Department) for a pre-syncopal episode.

 

QUESTION:

• Is this Wellens' Syndrome?

 

Figure-1: ECG obtained from a 30-ish year old man who presented to the ED for pre-syncope. Is this Wellens' Syndrome?

 

 

  — The Case Continues BELOW today's Audio Pearl ... —

 

 

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NOTE: Some readers may prefer at this point to listen to the 7:40-minute ECG Audio PEARL before reading My Thoughts regarding the ECG in Figure-1. Feel free at any time to refer to My Thoughts on this tracing (that appear below ECG MP-26a).

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Today's ECG Media PEARL #26a (7:40 minutes Audio) — Reviews what Wellens' Syndrome is — and what it is not (This is the revised version from 3/30/2021).

 

 

 

MY Approach to this Tracing:

As always — I favor a Systematic Approach for interpretation of every ECG I encounter (This Systematic Approach is reviewed in ECG Blog 205). The 1st Step in interpretation is Descriptive Analysis — which I find especially helpful for organizing your thoughts with complex tracings, such as the ECG shown in Figure-1. My Descriptive Analysis for this ECG is as follows:

• Rate & Rhythm: Although we lack a long lead rhythm strip — we can still say that the rhythm is slow (ie, ~60/minute) with slight-but-definite variation in the R-R interval. This is sinus arrhythmia. 
• Intervals: P waves are small in amplitude — but present and upright in lead II. The PR interval appears to be slightly short (ie, ~0.11-to-0.12 second in duration). The QRS complex is not prolonged — and the QTc is normal. NOTE: The isolated finding of a slightly short PR interval in a young adult is not necessarily a concerning finding. More clinical information is needed to assess this finding. As a result — I usually write "Short PR — Suggest clinical correlation" in my interpretation. It turns out that this slightly short PR interval was not relevant to today's case.
• Axis: The front plane axis is about +70 degrees, which is normal.

Chamber Enlargement: As noted earlier — P wave amplitude is reduced (ie, there is no sign of atrial enlargement). There is also no sign of RVH. Assessment of the ECG in Figure-1 for LVH (Left Ventricular Hypertrophy) is more challenging:

• QRS amplitude is often increased in younger adults (especially in men less than 35 years of age). As a result — It is difficult to arrive at a definite answer regarding the presence or absence of ECG criteria for LVH in this 30-ish year old man.
• That said, despite the young adult age of today's patient — QRS amplitude appears to be significantly increased — which I illustrate by coloring in overlapping QRS deflections in the anterior leads (Figure-2). QRS amplitude most probably satisfies voltage criteria for LVH given the very deep S waves in anterior leads V1 and V2 (or 18 mm and 23 mm, respectively) — with what appears to be an extremely deep S wave in lead V3 (which is cut off by the bottom of the paper after an S wave of 16 mm).
• NOTE: For more on the LVH voltage criteria that I favor — See ECG Blog #245.

 

 

Figure-2: For clarity — I have colored in overlapping QRS deflections in anterior leads V1, V2 and V3 (See text).

 

 

Regarding Q-R-S-T Changes:

• Slender but fairly deep Q waves are seen in each of the inferior leads (II, III, aVF). Slender Q waves are also seen in lateral chest leads V5, V6.
• R wave progression — reveals that R wave amplitude is surprising tall (ie, 9 mm) already by lead V1 — with an extremely tall R wave (of more than 20 mm) already by lead V2.

 

Assessment of ST-T waves:

• The most remarkable finding for the ST-T waves is seen in the anterior leads (ie, leads V1, V2 and V3). Each of these leads manifest ST segment coving with slight elevation — that leads into terminal T wave inversion.
• Less marked, nonspecific changes are seen in many of the remaining leads, including ST segment flattening and modest T wave inversion in lead III.
• There is ~2 mm of J-point ST elevation in leads V1 and V2. The T wave in lead V2 is biphasic with terminal negativity.

Clinical IMPRESSION:

The ECG in today's case shows sinus arrhythmia with borderline bradycardia — a slight short PR interval (of ~0.11-0.12 second) — marked increase in QRS amplitude that probably satisfies voltage criteria for LVH (despite the patient's young adult age) — and a clearly abnormal ST-T wave response in the anterior leads that resembles the ST-T wave appearance of Wellens' T waves.

• As alluded to earlier — chances are that the short PR interval has no bearing on today's case. Given the tiny P wave amplitude in lead II (that appears slightly smaller than the P wave in lead I) — this could be an ectopic atrial rhythm, which can be a normal variant. Depending on where within the atria the rhythm arises — the PR interval might normally be shorter (ie, if the ectopic atrial rhythm arose from an atrial site close to the AV node).

Why Wellens’ Syndrome is Unlikely in Today's Case:

I review the essentials of Wellens' Syndrome in today's ECG Media PEARL #26a (above) — and in the 2 Figures shown below in the Addendum. In a word, despite the presence of anterior ST-T wave changes that resemble those seen with Wellens' Syndrome — Today's case is unlikely to represent Wellens' Syndrome. This is because:

• As emphasized in my review of Wellens’ Syndrome — a history of recent chest pain that has now resolved is an essential part of the diagnosis. The patient in today's case is a younger adult (ie, therefore in a lower prevalence group for coronary disease) — and there is no mention of a history of preceding chest pain.
• The QT interval looks to be normal in Figure-2. In contrast — with Wellens' Syndrome, the QTc is often at least borderline prolonged.
• R wave amplitude in the anterior leads is markedly increased (ie, the R wave in lead V1 is ~9 mm — and the R wave in lead V2 is huge at 24 mm!). Most cases of Wellens' Syndrome are associated with reduced anterior R wave amplitude, often with delayed transition in the chest leads.
• There is voltage for LVH. The diagnosis of Wellens' Syndrome should be made with caution in the presence of marked increase in QRS amplitude — because of the tendency for this to produce false positive results.
• Overall — The ECG pattern of increased voltage, early transition and ST-T wave changes similar to those in Figure-2 is commonly seen as a repolarization variant in younger adults. By exclusion — follow-up in today's case suggested this (and not Wellens' Syndrome) to be the explanation for the ECG findings in Figure-1. So YES — Clearly evaluation of this patient was indicated, because the ECG pattern in Figure-1 could potentially be consistent with either LVH or HCM (Hypertrophic CardioMyopathy) — But Echo showed neither LVH nor HCM.

 

 

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ADDENDUM (10/1/2021): In the following 2 Figures — I post written summary from my ECG-2014-ePub regarding Wellens’ Syndrome. 

• CLICK HERE — for a PDF of this 3-page file on Wellens’ Syndrome that appears in Figure-3 and Figure-4.

 

 

Figure-3: Regarding Wellens’ Syndrome (from my ECG-2014-ePub).

Figure-4: Wellens’ Syndrome (Continued). 

 

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Acknowledgment: My appreciation to Ghady Rahhal (from Virginia, USA) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case: 

ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation (outlined in Figures-2 and -3, and the subject of Audio Pearl MP-23 in Blog #205).

 

ECG Blog #209 — Reviews a case of marked LVH that results in similar ST-T wave changes as may be seen with Wellens' Syndrome.

 

ECG Blog #245 — Reviews my approach to the ECG diagnosis of LVH (outlined in Figures-3 and -4, and the subject of Audio Pearl MP-59 in Blog #245).

ECG Blog #253 (67) — PVCs or Aberrant Conduction?

The 2 tracings that are shown in Figure-1 and Figure-2 were obtained during and shortly after a screening ETT ( = Exercise Treadmill Test).

 

QUESTIONS:

• Are the earlier-than-expected wide beats in both tracings PVCs (Premature Ventricular Contractions) or PACs (Premature Atrial Contractions) with aberrant conduction?
• What are the clinical implications of these early wide beats?

 

Figure-1: 12-lead ECG and dual-lead rhythm strip obtained from an ETT during exercise (See text).

 

Figure-2: 12-lead ECG and dual-lead rhythm strip obtained from an ETT after exercise (See text).

 

  — The Case Continues BELOW today's Audio Pearl ... —

 

 

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NOTE: Some readers may prefer at this point to listen to the 11:15-minute ECG Audio PEARL before reading My Thoughts regarding the ECGs in Figure-1 and Figure-2. Feel free at any time to refer to My Thoughts on these tracings (that appear below ECG MP-67).

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Today's ECG Media PEARL #67 (9:10 minutes Audio) — Applies the wisdom from 2 of my favorite sayings to the "art" of ECG interpretation. These 2 sayings are = "Birds of a Feather" and "Forest from Trees".

 

 

 

Some Brief Concepts on ETT Basics:

Performing and interpreting ETTs is a skill that extends beyond the scope and purpose of my ECG Blog. That said — review of the 2 tracings in Figure-1 and Figure-2 illustrates some important concepts very relevant to distinction between PVCs vs aberrantly conducted PACs.

• The principle of Exercise Treadmill Testing (ETT) is simple: The patient performs a progressively increasing degree of exercise on a moving treadmill while the clinician monitors a series of parameters, including hemodynamic factors (ie, heart rate, blood pressure) — ST-T wave response to exercise — the cardiac rhythm — and the patient's tolerance for increasingly demanding exercise (ie, Assessing the patient for development of chest pain, shortness of breath, dizziness, fatigue, etc.).
• Much more than just the ST segment response to exercise is monitored. It is true that the ECG finding of flat or downsloping ST depression in a patient who develops chest pain with no more than low-level exercise during the ETT is a clear indication for prompt cardiac catheterization. But so much more can be learned! For example, the patient who denies all symptoms during the ETT — but who looks to be obviously fatigued at low-level exercise with development of associated arrhythmias and hypotension is at even higher risk of an acute cardiac event — because that patient lacks a "warning system" (ie, It is likely that such a patient will develop and deny fatigue with associated hypotension and arrhythmias during low-level activities of daily living — which poses a real risk of cardiovascular collapse if activity is continued).
• The treadmill always wins. By progressively increasing the speed and degree of incline of the treadmill — even the most athletically fit individual will eventually fatigue. And THAT is one of the goals of performing an ETT (or "Stress" Test) — namely, that you want to see the ECG response to exercise when your patient is subjected to a level of activity at least comparable (if not exceeding) what that person does every day in an unmonitored situation at home.
• The final point I'll make relates to the purpose of the ETT in today's case — which was as a screening test to assess this asymptomatic patient for exercise capacity and exercise prescription. How intense of an exercise effort will be appropriate for this patient? Insight into an individual's suitability for a given degree of unsupervised exercise can be gained from their performance on the ETT.
•  
• NOTE: For those interested — In 1998, I wrote a user-friendly manual regarding the basics of performing and interpreting ETTs in the office (which I did and taught for years). Realizing that this manual is now 20+ years old ... the basic principles are still valid. CLICK HERE for FREE download of my ETT Pocket Brain PDF (Linked Contents in the PDF Bookmarks facilitate a quick overview of the subject).

 

 

My Sequential THOUGHTS on Today's Case:

Realizing that we lack historical details about the patient in today's case — as well as not knowing for how long he/she exercised on the treadmill, nor their physiologic response — we still can interpret these 2 tracings with regard to the etiology of the early ectopic beats:

 

ECG #1 — Obtained during Exercise:

• The underlying rhythm appears to be sinus tachycardia at a rate close to ~150/minute. Although we do not know the age of the patient, nor the stage of exercise during the ETT that Figure-1 was obtained — the chances are good that at the least — a reasonable degree of exercise has been achieved by the test (ie, probably at least 85% of maximal predicted heart rate for age).
• A number of wider beats are seen in Figure-1. The 2 most obvious wide beats are seen in simultaneously-obtained leads V1, V2 and V3 (ie, beats #15 and 19).
• Looking at the long lead rhythm strips (of lead II and lead V5) — at least a few other wider (different-looking) beats are seen (ie, beats #7, 11, 23). 
• Each of the different-looking beats occur a little bit early! That said — I could not tell from Figure-1 if these wider (different-looking) beats were PVCs or PACs with aberrant conduction.
• Clinically — it would not matter if these slightly early, different-looking beats were PVCs or aberrantly conducted PACs because: i) The ST segment response in Figure-1 shows no more than a minimal amount of rapid-upsloping ST depression, which is a normal (non-ischemic) response to exercise; and, ii) If the patient was appropriately tolerating the amount of exercise — PVCs at the frequency seen here, that do not occur in runs are not necessarily an indication to stop the test.
• ETT NOTE: Fusion beats are common during exercise testing. This is because as heart rate increases — the R-R interval correspondingly decreases, which means there is a much greater chance for the occurrence of any PVCs that are seen to coincide with sinus-conducted beats. This explains why beats such as #7, 11 and 23 that do not look extremely wide may nevertheless represent PVCs (ie, if these beats are fusion beats).
• ETT NOTE: In general, the amount of artifact increases at increasing degrees of exercise — because the patient is having to walk up an ever increasing incline at faster and faster speeds. As a result — rhythm interpretation and assessment of the ST segment response to exercise may be challenging. This is why the most helpful tracing for assessing ST-T wave changes during ETT is usually the immediate post-Exercise tracing — because the heart rate will still be fast, with great reduction in the amount of artifact compared to tracings obtained during exercise.

 

ECG #2 — Obtained after Exercise:

• ETT NOTE: ECG monitoring is usually continued for between 6-10 minutes after the completion of maximal exercise (unless the patient is still having symptoms or arrhythmias after this period of time). ST segment depression that only occurs at peak exercise, and is not accompanied by chest pain — and, which promptly resolves in recovery (ie, within 2-4 minutes after stopping the test) is less likely to indicate significant underlying coronary disease.
• Although we are not told when during the post-exercise period ECG #2 was obtained — the fact that the sinus rate is barely over 100/minute in ECG #2 (compared to ~150/minute in ECG #1) suggests that at least several minutes have already passed in the recovery period after stopping the test. That said — there are still frequent wider (different-looking) beats, as is best seen in the long lead II and V5 rhythm strips in Figure-3.
• Sinus P waves are highlighted by RED arrows in Figure-3. Note that different-looking QRS complexes occur every 4th beat (ie, Beats #2, 6, 10 and 14 in Figure-3 are each wider and very different-looking compared to the other sinus-conducted beats in this tracing).
• Note that there are 2 different QRS morphologies for the wider beats in Figure-3, that I have labeled X1 and X2. The KEY for determining the etiology of these wider beats is highlighted by the YELLOW arrows in the long lead II rhythm strip. There is an unmistakeable notch under each of these YELLOW arrows that is not present either in or just after the T wave in the other sinus-conducted beats (ie, No notch is seen over the vertical BLUE lines in the long lead II rhythm strip). This proves that these YELLOW arrows each highlight a premature P wave (PAC), that precedes each of the wider beats in the long lead II rhythm strip in Figure-3.
• PEARL #1: The best clue that a wider, different-looking early beat is an aberrantly conducted PAC — is when this beat is preceded by a PAC (which it is in Figure-3, as proved by the notch under each of the YELLOW arrows).
• PEARL #2: The next best clue in favor of aberrant conduction is the finding of a QRS morphology for the wider, different-looking beats that resembles some form of known conduction defect. Note that QRS morphology for each of the wider beats labeled X1 in Figure-3 is consistent with LBBB conduction (ie, upright [albeit notched] QRS in lateral leads I, V5 and V6 — and predominantly negative QRS with extremely steep S wave downslope for beat #10 in lead V1).
• Bottom Line: The underlying rhythm in Figure-3 is sinus with atrial quadrigeminy — in which every 4th P wave is a PAC (YELLOW arrows) that conducts with LBBB aberration (X1 beats).

 

 

Figure-3: I have labeled ECG #2 to highlight key features of the different-looking beats (See text).

 

 

Taking Another Look at ECG #1 — Obtained during Exercise:

• In Figure-4 — I have labeled the slightly early, different-looking beats from Figure-1 with either an X1 or X2 notation — corresponding to the 2 different QRS morphologies that we identified in Figure-3.
• As previously stated — the rapid rate and amount of artifact induced by exercise made it extremely difficult to confidently identify premature atrial activity in ECG #1. That said — we still can assess QRS morphology for the 2 clearly widened beats in simultaneously-obtained leads V1, V2, V3 of Figure-4.
• The beat in lead V1 that is labeled X1 (in Figure-4) manifests a predominantly negative QRS with very steep S wave downslope that looks identical to QRS morphology of beat #10 in lead V1 in Figure-3. 
• QRS morphology in the long lead V5 rhythm strip for the 3 complexes labeled X1 in Figure-3 manifests a notched-R morphology. This is similar to the notched-R morphology in the long lead V5 rhythm strip for beat #15 in Figure-4. So, even though we are not able to identify a premature P wave before beat #15 in the long lead V5 of Figure-4 (because of all the artifact produced during exercise) — it is likely that the etiology of this X1 beat in Figure-4 is the same as the etiology that we proved for the 3 X1 complexes in Figure-3 ( = aberrantly conducted PACs).
• Taking another look at beat #19 in Figure-4 (that we have labeled with an X-2 notation) — there is an rsR' morphology for this beat #19 in lead V1, in which the S wave descends below the baseline — and the R' is slender and manifests a taller right "rabbit ear". This QRS morphology for beat #19 in lead V1 is extremely typical for RBBB aberration — which is supported by the finding of a wide terminal S wave for this same beat #19 in the long lead V5 rhythm strip.
• PEARL #3: By the "Birds of a Feather" concept (See the above Audio Pearl #67) — Since the "theme" of the slightly early, different-looking beats in these 2 tracings is that these are aberrantly conducted PACs (as proven by the YELLOW arrows that highlight premature P waves!) — the chances are that other slightly early, different-looking beats are also aberrantly conducted supraventricular impulses (and not PVCs). 

 

CONCLUSION: These 2 tracings, taken from a screening ETT — provide an insightful example of how careful observation allows identification of subtle-but-evident premature P waves (PACs) that confirm a supraventricular etiology for the sighty early, different-looking beats. 

• PACs are conducted with varying degrees of RBBB and LBBB aberration. 
• The modest amount of rapid-upsloping ST depression during exercise, that resolves in recovery suggests a negative screening test for ischemia (although clearly, additional details about the patient and specifics on exercise parameters during each stage of the test would be needed for full analysis).

 

Figure-4: I have labeled ECG #2 to highlight key features of the different-looking beats (See text).

 

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Acknowledgment: My appreciation to Massimo Bolognesi (from Cesena, Italy) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #128 — Reviews the concept of Fusion Beats.
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• ECG Blog #211 — Reviews why some beats (and rhythms) are conducted with aberration (and why the most common form of aberrant conduction manifests RBBB morphology). 
• ECG Blog #33 — Reviews a case showing blocked and aberrantly-conducted PACs. 
• ECG Blog #66 — Reviews a case showing blocked and aberrantly-conducted PACs. 
• ECG Blog #140 — Reviews a case showing PACs with varying aberrant morphology.