ECG Blog #430 — Just a Regular LBBB ECG?

The ECG in Figure-1 — was obtained from an older man who had just completed dialysis — and, is now complaining of abdominal discomfort that radiates to his chest.

• The consultant interpreted this tracing as “LBBB” (Left Bundle Branch Block) — but not indicative of anything acute.

QUESTIONS: 

• Do you agree with the consultant’s interpretation?
• How would YOU approach this case?

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

MY Initial Thoughts on Today’s CASE:

Given the older age of the patient in today’s case — and, the fact that he just completed dialysis — the chance of having underlying coronary disease is clearly increased. This patient's new complaint of pain that radiates to his chest therefore immediately places him in a “higher-prevalence” group for having an acute event (especially since hemodialysis is a procedure in which transient hypotension is not uncommon).

• For clarity in Figure-2 — I’ve labeled today’s initial ECG. The rhythm is sinus at ~85/minute (the RED arrow highlighing the upright P wave in lead II). The QRS complex is wide — with a morphology most consistent with LBBB ( = predominantly upright in left-sided leads I and aVL — and predominantly negative in the anterior leads).
• Serum K+ was normal. 
• 
  
• NOTE: By my observation over the years — the experts do not agree on the classification of LBBB vs IVCD (IntraVentricular Conduction Defect). As I review in ECG Blog #204 — “typical” LBBB is characterized by a supraventricular rhythm with QRS widening, in which there is a monophasic R wave in left-sided leads I and V6 — and an all-negative (or almost all negative) QRS in right-sided lead V1. 
• The above said — many patients with LBBB also have marked LVH. Given the leftward and posterior orientation of a markedly enlarged LV (Left Ventricle) — the presence of an all-upright R wave may not be seen in left-sided lead V6. Instead, the all-positive R wave with LBBB may sometimes only appear in more lateral and posteriorly-oriented chest leads, such as V7,V8 or V9.
• As a result — I would accept either LBBB or IVCD as a “correct” classification of the widened QRS morphology seen in Figure-2. Personally, I favor LBBB in view of the suggestive appearance of LBBB in the limb leads, with fairly deep anterior S waves — but my comments below are consistent with either LBBB or IVCD.

PEARL #1: Regardless of whether you interpreted the widened QRS morphology in today’s ECG as “LBBB” or “IVCD” — there are a number of ECG findings of increased concern beyond that of the conduction defect. Among them: 

• There should never normally be a Q wave in a lateral lead with simple LBBB. As discussed in ECG Blog #204 — this is because by definition, the conduction defect with LBBB prevents normal left-to-right septal depolarization. The same is true for an IVCD pattern that mimics LBBB in the limb leads (as is seen in today’s ECG). Therefore — the Q waves in Figure-2 (BLUE arrows in leads I and aVL) suggest that in addition to the conduction defect — there is also “scar” (usually from infarction at some point in time).

In addition to the abnormal Q waves — ST-T wave morphology is distinctly abnormal in almost every lead!

• While more difficult to assess because of the lack of an all-upright R wave in lateral lead V6 — the shape of the ST-T waves in multiple leads is just not normal.
• BLUE lines in leads V2,V3 show abnormal ST segment straightening (instead of the expected upsloping ST segment in these leads).
• PURPLE lines in leads V4,V5,V6 show abnormal downsloping ST segments (with marked abnormal ST depression in leads V5,V6). In addition — the biphasic T wave with marked terminal positivity in leads V5,V6 looks distinctly acute (ie, T waves are not normally upright in lateral chest leads with LBBB).
• Similar downsloping with marked, abnormal ST depression and abnormal biphasic T wave with marked terminal positivity — is seen in lead II.
• While ST segments in leads III and aVF are not nearly as depressed or downsloping (as they are in lead II) — the ST segment straightening that we see in leads III and aVF, with marked angulation at the point where the ST segment meet the beginning of the T wave — is clearly not normal.
• Finally — note how marked the ST elevation is in lead aVR (within the RED box in this lead).

Putting It All Together:

The older man in today’s case was clearly in a higher-prevalence group for an acute event — even before we looked at his initial ECG. As a result — there was need to assume that any potentially abnormal ECG findings that might be seen are acute until proven otherwise.

• In summary, the ECG in Figure-2 shows sinus rhythm with LBBB — and diffusely abnormal ST-T wave depression with ST elevation in lead aVR. At the least — this pattern is consistent with DSI (Diffuse Subendocardial Ischemia — See ECG Blog #271 for more on DSI).
• More than this — the Q waves in leads I and aVL — and the acute appearance of the downsloping ST depression with terminal T wave positivity — might reflect multi-vessel disease with recent and/or ongoing acute infarction.
• 
  
• Finding a prior tracing on this patient would be extremely helpful — as it would tell us what is "new" vs old.
• Obtaining serial ECGs should prove insightful. Especially when correlated to the presence and relative severity of symptoms — serial tracings will convey if acute injury is ongoing. For example — a reduction in symptoms in association with improvement in ST-T wave changes, would suggest that the "culprit" vessel is spontaneously opening!
• PEARL #2: In patients with ongoing symptoms — ST-T wave elevation and reciprocal ST depression may evolve over a period of minutes. As a result — Consider a repeat ECG as often as every 10-to-20 minutes in a patient with ongoing CP (Chest Pain) — until a definitive diagnosis can be made.
• 
  
• BOTTOM Line: On seeing today's ECG — prompt cath was clearly indicated.

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

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Acknowledgment: My appreciation to Mayan Kain (from Tel Aviv, Israel) 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.
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• ECG Blog #193 — Reviews the basics for predicting the "culprit" artery (as well as reviewing why the term "STEMI" — should be replaced by "OMI" = Occlusion-based MI).

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• CLICK HERE — for my 6 new ECG Videos (on Rhythm interpretation — 12-lead interpretation with Case Studies for ECG diagnosis of acute OMI).
• CLICK HERE — for my 2 new ECG Podcasts (on ECG & Rhythm interpretation Errors — and — Errors in assessing for acute OMI).

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• Recognizing hyperacute T waves — patterns of leads — an OMI (though not a STEMI) — See My Comment at the bottom of the page in the November 8, 2020 post on Dr. Smith's ECG Blog.
• Recognizing ECG signs of Precordial Swirl (from acute OMI of LAD Septal Perforators) — See My Comment at the bottom of the page in the March 22, 2024 post on Dr. Smith's ECG Blog. 
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• ECG Blog #294 — Reviews how to tell IF the "culprit" artery has reperfused.
• ECG Blog #230 — Reviews how to compare serial ECGs. 
• ECG Blog #115 — Shows how dramatic ST-T changes can occur in as short as an 8-minute period.
• ECG Blog #268 — Shows an example of reperfusion T waves.
• ECG Blog #400 — Reviews the concept of "dynamic" ST-T wave changes.
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• ECG Blog #337 — A "NSTEMI" that was really an ongoing OMI of uncertain duration (presenting with inferior lead reperfusion T waves).
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• ECG Blog #282 and ECG Blog #204 — review a user-friendly approach to the ECG diagnosis of the Bundle Branch Blocks (RBBB, LBBB and IVCD).
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• ECG Blog #203 — reviews ECG diagnosis of Axis, Hemiblocks and Bifascicular Blocks.

 

ECG Blog #429 — Mobitz I or Mobitz II?

The 12-lead ECG and long lead II rhythms shown in Figure-1 — was obtained from an older man with a recent history of “easy fatiguability” and a presyncopal episode.

QUESTIONS:

• How would YOU interpret the ECG in Figure-1?
• Is the group beating due to the Mobitz I or Mobitz II type of 2nd-degree AV block?

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

MY Initial Thoughts on Today’s CASE:

For clarity, given the above clinical history — I present my initial thoughts regarding clinical interpretation of today’s initial ECG in the sequence I used for assessment of this case. 

• To EMPHASIZE: One of my goals in developing this ECG Blog — is to help clinicians to optimize their time efficiency. For example, in today's case — I completed my initial assessment of the tracing in Figure-1 in less than 1 minute. I outline my approach for doing so below. 

MY Approach:

When presented with a 12-lead ECG and accompanying long-lead rhythm strip — I favor spending a few quick seconds first taking a look at the long lead rhythm strip — before I look at the 12-lead. This is especially relevant when either the QRS is wide and/or the rhythm is not regular (and in today’s case — both of these conditions are present!).

• By the Ps, Qs, 3R Approach (See ECG Blog #185) — the rhythm in the long-lead II of Figure-1 is not Regular. Instead — there is a pattern consistent with “group beating” (ie, groups of 2 beats — each with similar spacing between these 2 beats — and — similar spacing during the slight pause between groups).
• The QRS complex in the long lead II appears to be wide (ie, more than half a large box on ECG grid paper — and in Figure-1, at least 0.12 second).
• P waves are present in front of each of the 13 beats in the long-lead II rhythm strip (RED arrows in Figure-2). These P waves are all upright in this lead II — with a constant and normal PR interval (ie, all P waves are Related to the QRS closest to them — in that the PR interval remains the same before all beats). There is therefore an underlying sinus rhythm in today's tracing.
• The 5th parameter in the Ps,Qs,3R Approach is the 3rd R = Rate — which is difficult to determine because of the irregularity in the rhythm. That said — we can say that the rate is not overly fast.
• 
  
• To EMPHASIZE: Assessment of today’s rhythm by the approach outlined in the above bullets should take less than 30 seconds! The conclusion I came to (within these 30 seconds) — was that today’s rhythm manifests conduction of sinus beats at a reasonable heart rate — with a wide QRS and with group beating.

Figure-2: I've labeled sinus P waves with RED arrows.

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PEARL #1: For as interesting as the rhythm in today’s case looks to be (ie, with group beating and a wide QRS) — I’ll suggest that optimal time efficiency for clinical assessment and management — would be to next figure out WHY the QRS complex is wide!

• As noted above — there is sinus conduction in today's rhythm, with a constant and normal PR interval. As a result — there is no WPW. This means the cause of the wide QRS in today's rhythm is due to some type of conduction defect.
• 
  
• As reviewed below in today's ADDENDUM — attention to 3 KEY leads ( = right-sided lead V1 — and left-sided leads I and V6) — allows you to distinguish between the 3 principal types of conduction defects within seconds!
• Normally — the QRS is predominantly negative in right-sided lead V1. Therefore — the combination of the widened RR' complex seen in lead V1 of Figure-2 — in association with the wide terminal S waves seen in left-sided leads I and V6 — is diagnostic of RBBB (Right Bundle Branch Block) as the explanation for QRS widening in today's case (See ECG Blog #282 for review on ECG diagnosis of the BBBs).

PEARL #2: The ECG Video in today's ADDENDUM also reviews quick assessment of ST-T wave changes in bundle branch block. The simple rule that can be assessed within seconds, is that with either RBBB or LBBB — the ST-T wave in the 3 KEY leads (leads I, V1, V6) will be oppositely directed to the last QRS deflection in these 3 leads.

• Since the last QRS deflection in lead V1 of Figure-2 is positive (ie, the R' ) — the ST-T wave in this lead should be negative. It is.
• Since the last QRS deflection in lateral leads I and V6 is the negative S wave — the T wave in these leads should be positive. It is.
• 
  
• Looking next at neighboring leads in Figure-2 — there appear to be no acute ST-T wave changes.

Next — A closer look at the Rhythm ... 

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PEARL #3: Despite the title of today’s blog post (which is, "Mobitz I or Mobitz II?" ) — We can tell at a glance that today’s rhythm does not represent any form of AV block — because the atrial rate is not regular!

• Using calipers tremendously expedites the process. With 2nd- or 3rd-degree AV block — the atrial rate should be regular (or at least almost regular — if there is an underlying sinus arrhythmia) — but it should be clear from the timing of the RED arrows in Figure-2 — that no on-time P wave occurs between beats #1-2; #3-4; #5-6; #7-8; #9-10; #11-12.
• 
  
• For completeness, I'll note that SA Block can produce the bigeminal pattern of beats that we see in Figure-2 . That said, as emphasized in ECG Blog #312 — SA block is rare! I count on my fingers and toes the number of times I've seen true SA block over my decades of diligently looking for this rhythm disorder. 
• 
  
• Instead, as suggested in PEARL #4 — there is a much more common explanation for today's arrhythmia that we should look for first!

PEARL #4: Perhaps my favorite mantra in arrhythmia interpretation is the following statement that I learned from Marriott: "The most common cause of a pause is a blocked PAC."

• In clinical practice, when confronted with a "pause" in the rhythm — the finding of blocked PACs is far more common than any form of AV block. 
• To emphasize, that by a "pause" — I mean any even slightly longer-than-expected interval, which clearly is present in Figure-2 — because the interval between the 2-beat groups is much longer than anticipated given the P-P interval between the RED arrow sinus P waves in this tracing.
• As a result, as soon as I saw the bigeminal rhythm in today's case (ie, with brief pauses between each of the 2-beat groups) — I considered the possibility of blocked PACs.

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Now — Take another LOOK at Figure-2.

• Carefully examine the ST-T wave of every odd-numbered beat in Figure-2 — and compare these ST-T waves with the the ST-T waves of each even-numbered beat. 
• 
  
• Is there any difference?

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I illustrate my ANSWER in Figure-3:

Figure-3: Is there any difference in the ST-T waves?

Figure-3 Explained:

The challenge in looking for blocked PACs — is distinguishing between subtle differences in ST-T waves that are "real" vs artifact vs slight variations that can normally be seen in parts of the tracing.

• Isn't the ST-T wave of every even-numbered beat in Figure-3 straighter (above the slanted BLUE lines) — than the ST-T wave of every odd-numbered beat (above the slanted RED lines)? That's because there is a non-conducted PAC that is hidden within the ST-T waves of every odd-numbered beat — and this is what causes this slight-but-real distortion of the ST segment! These blocked PACs serve to "reset" the SA node — and thereby produce the slight pause that we see between each of the 2-beat groups!
• 
  
• PEARL #5: It's important to appreciate that PACs that arise from a site close to the SA node may look similar in morphology to sinus P waves. For this reason — I always look at simultaneously-recorded leads for subtle differences in P wave morphology that might not be readily apparent on a single long lead rhythm strip. NOTE: YELLOW arrows in Figure-3 show that the difference in ST-T wave morphology between sinus-conducted beats and the beats with blocked PACs is most easily seen in leads V2 and V3.

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The Lesson I Learned a Long Time Ago ...

• As emphasized earlier in PEARL #4: The most common cause of a pause is a blocked PAC. Blocked PACs are much common than any form of AV block.
• Until I became aware of the fact that blocked PACs are the most common cause of a pause — I never saw blocked PACs.
• Once I began to look for blocked PACs — I found them everywhere!
• 
  
• Remember that the biggest challenge in accurately diagnosing blocked PACs — is distinguishing between differences in ST-T waves that are "real" vs artifact vs slight variations that can normally be seen in parts of the tracing. 
• KEY Point: In today's case — the reason I know that the differences in ST-T wave morphology between odd- and even-numbered beats is real — is because it is seen with every beat in the long lead rhythm strip in Figure-3.

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Acknowledgment: My appreciation to Hafiz Abdul Mannan Shahid (from Lahore, Pakistan) for the case and these tracings.

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 Related ECG Blog Posts to Today’s Case: 

• ECG Blog #185 — Reviews the Ps, Qs and 3R Approach to Systematic Rhythm Interpretation.
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• ECG Blog #232 — Reviews the causes of Bigeminy.
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• ECG Blog #164 — Reviews a case of Mobitz I 2nd-Degree AV Block, with detailed discussion of the "Footprints" of Wenckebach.
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• ECG Blog #252 — for a similar case as today (with LINKS to more examples of blocked PACs).

 

 

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ADDENDUM (5/11/2024): I've added below material regarding a user-friendly approach to the ECG diagnosis of the Bundle Branch Blocks

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ECG Media Pearl #22 (13:15 minutes Video) — Reviews a user-friendly approach that allows diagnosis of the Bundle Branch Blocks in less than 5 seconds. 

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• CLICK HERE — for FREE download PDF of this 26-page file on BBB (from my ECG-2014-ePub) — with review on the Basics for ECG diagnosis of the Bundle Branch Blocks (including diagnosis of acute MI & LVH with BBB).

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ECG Blog #428 — How Much to Do at Age 92?

I was sent the tracing in Figure-1 — with the following information:

• 92-year old patient with a history of "known arrhythmia" and hypertension.
• The patient was asymptomatic at the time ECG #1 was obtained — with the ECG presumably being recorded because an irregular rhythm was heard on auscultation. 

QUESTIONS:

• How would YOU interpret the rhythm in Figure-1?
• How much should we do for this 92-year old patient?
• 
  
• Extra Credit: Which arm or leg is most responsible for the artifact seen in today's initial ECG?

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

Answer to EXTRA Credit Question:

To begin with the answer to the Extra Credit Question — I suspect the cause of the abnormal baseline deflections seen in Figure-1 is muscle tremor artifact (See Bouthillet T — ACLS Med Training, Dec, 2015). A quick LOOK at the patient would confirm this — but I unfortunately do not have any information about the patient's appearance.

• NOTE: The abnormal baseline deflections in Figure-1 are maximal in leads I,III and aVL — modest in lead aVF — and minimal in lead II, as well as being minimal in the 6 chest leads. Therefore — the "culprit" extremity most responsible for the artifact in today's tracing is the LA (Left Arm).
• 
  
• As discussed in detail in ECG Blog #255 — We can identify the "culprit" extremity because the relative size of the artifact deflections in Figure-1 manifest the relative dimensions expected when a single extremity is primarily responsible for a certain type of artifact.
• 
  
• PEARL #1: That one extremity is primarily responsible for a certain type of artifact — can be quickly recognized by the finding of approximately equal artifact amplitude in 2 of the 3 standard limb leads (ie, in leads I and III for Figure-1) — and, minimally or not seen at all in the 3rd standard limb lead (ie, artifact is minimal in lead II). 
• By Einthoven’s Triangle (See ECG Blog #255) — the finding of equal artifact amplitude in Lead I and Lead III, localizes the “culprit” extremity to the LA ( = Left Arm) electrode.
• The greatly reduced artifact amplitude in lead II is consistent with this — because, derivation of the standard bipolar limb lead II is determined by the electrical difference between the RA ( = Right Arm) and LL ( = Left Leg) electrodes, which are not affected if the source of the artifact is the left arm.
• 
  
• SHORTCUT (To find the "culprit" extremity in seconds!): When 2 of the standard limb leads show approximately equal maximal artifact amplitude — and the 3rd standard limb lead shows minimal or no artifact — then whichever augmented lead shows maximal amplitude indicates the "culprit" extremity (which in Figure-1 is Lead aVL = which means that the LA is the "culprit" extremity).

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Back to Today's CASE:

• How would YOU interpret the rhythm in Figure-1?
• How much should we do for this 92-year old patient?

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

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MY Initial Thoughts:

From an arrhythmia standpoint — I found the rhythm in today's case to be fascinating. 

• That said — this patient is elderly and asymptomatic, which raises the questions as to, How much evaluation? — and — What clinical management would be optimal?

We are told in the brief information given — that today's patient has a history of a "known arrhythmia". Thus, the 1st issue that comes to mind in today's case is — What is the arrhythmia that this patient is "known" to have?

• By far — the most common cause of an irregularly rhythm in an asymptomatic elderly patient is AFib (Atrial Fibrillation).
• IF this patient had AFib — then determination of the need for rate control and/or informed consent by the patient (and/or by the family, if the patient is no longer mentally competent) regarding the pros and cons of anticoagulation — would be indicated.
• The above said — I was not made aware of additional specifics of this patient's medical history — and, the rhythm in today's case is not AFib.

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HOW to Interpret Today's Rhythm:

The "good news" — is that the elderly patient in today's case is asymptomatic. This means that we have at least a moment of time to try to figure out the rhythm in Figure-1. My initial observations include the following:

• The rhythm is obviously irregular. 
• There are 2 different QRS morphologies. These are: i) Beats #1-thru-4; beat #11; and beats #15,16 — all of which are at most, boderline prolonged, with an rS configuration in the long lead II rhythm strip; and, ii) The remaining 10 beats — all of which are of normal QRS duration, and manifest an RS configuration in the long lead rhythm strip.
• 
  
• The first 4 beats are regular at a rate of ~95-100/minute — and, they are not preceded by P waves. These first 4 beats manifest marked LAD (Left Axis Deviation) — being positive in lead I — but virtually all negative in simultaneously-recorded leads II and III.
• Beats #11 and #15,16 manifest an incomplete RBBB morphology (ie, with a nearly equiphasic R=S for beat #11 in lead V1 — and, with wide, terminal S wave for beats #15,16 in lead V6). This combination of incomplete RBBB + LAHB morphology for beats #1-thru-4; beat #11; and beats #15,16 — suggests that these 7 QRS complexes are all fascicular beats that arise from the LPH (Left Posterior Hemifascicle).
• NOTE: Since fascicular beats are ventricular beats — this means that the first 4 beats in Figure-1 constitute a short run of NSVT (Non-Sustained Ventricular Tachycardia), albeit an NSVT at the modest rate of ~95-100/minute.
• 
  
• The remaining 10 beats in Figure-1 manifest a narrow QRS complex in all 12 leads — and, are therefore supraventricular.

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QUESTION: 

• In Figure-1 — Is the underlying rhythm sinus?
• 
  
•     HINT: Is there a predominant P wave morphology?

ANSWER: The easiest way to tell if an underlying sinus rhythm is present — is to LOOK for: i) A predominant P wave morphology (ie, in which the P wave in lead II is upright with a constant PR interval); and, ii) A consistent R-R interval before the predominant P wave morphology. 

• As can be seen in Figure-2 — it appears that both of these features are present in today’s rhythm.

Figure-2: I've labeled sinus P waves with RED arrows.

NOTE in Figure-2 — The underlying rhythm is sinus!

• RED arrows in Figure-2 highlight what appear to be similar-looking upright P waves in the long lead II rhythm strip. At least before beats #6, 7 and 9 — the preceding R-R interval is very similar, suggesting these 3 P waves represent normal sinus-conducted beats.

Now that we have identified that, with the exception of fascicular beats #1-4; 11; 15,16 — the underlying rhythm in today's tracing is sinus — We can focus our attention on the remaining beats in today’s tracing:

• Beats #5; 8; 12; 13; and 17 — all occur earlier-than-expected — are all preceded by a P wave with a P wave morphology that is different from that of the RED arrow P waves — yet all manifest the same supraventricular QRS morphology as the 3 sinus-conducted beats ( = beats #6,7,9). 
• These 5 beats ( = beats #5,8,12,13,17) — are therefore PACs (Premature Atrial Contractions).

Putting It All Together:

I summarize in Figure-3 — what we have thus far determined for today’s arrhythmia:

• There are 2 distinct QRS morphologies in today’s rhythm.
• Beats #1,2,3,4 — beat #11 — and beats #15,16 — represent the first QRS morphology, in which there is slight QRS widening with a pattern consistent with incomplete RBBB/LAHB conduction. Based on the regularity of beats #1-thru-4, and the absence of sinus P waves in front of these 4 beats — these must be fascicular beats from the LPH.
• Since QRS morphology of beats #11,15,16 is so very similar to that of beats #1,2,3,4 in the long lead II rhythm strip — all of the beats marked by a RED circle in Figure-3 are fascicular beats.
• The finding of 4 consecutive beats of ventricular etiology at an accelerated rate — means that beats #1-thru-4 represents a 4-beat run of NSVT.
• YELLOW arrows highlight a negative deflection occurring just after the QRS of these first 4 beats. Because no such negative deflection follows the QRS of the other 3 fascicular beats (each of which is preceded by a RED arrow sinus P wave) — we know that the 4 YELLOW arrows in Figure-3 must represent 1:1 VA conduction (ie, retrograde P waves) that follow these first 4 fascicular beats.

Figure-3: Further labeling of today's tracing.

Additional Findings in Today's Rhythm:

As noted earlier — the underlying rhythm in today's tracing is sinus, since there is a predominant P wave morphology in the form of similar-looking upright P waves with constant PR interval in front of beats #6,7; 9,10; 14 (RED arrow P waves in front of these beats in the long lead II rhythm strip).

• PEARL #2: Seemingly on-time RED arrow P waves also appear in front of fascicular beats #11,15,16 — but with a shorter PR interval. This observation provides further support that beats #11,15,16 are of ventricular etiology (ie, The shorter PR interval of these on-time RED arrow P waves represents transient AV dissociation).
• 
  
• PEARL #3: Did YOU notice the slightly smaller S wave amplitude of fascicular beat #11? The reason for this — is that beat #11 is a fusion beat (ie, the RED arrow P wave in front of beat #11 partially conducts — resulting in "fusion" between fascicular beat morphology and the RS morphology of supraventricular beats). As per ECG Blog #128 — identification of fusion beats in this setting proves a ventricular etiology.
• 
  
• Finally in Figure-3 — I've selected different colors to represent the different P wave morphologies of the 5 PACs (colored P wave arrows before beats #5,8,12,13,17).

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LADDERGRAM Illustration:

For clarity — I offer my proposed laddergram in Figure-4.

• RED arrows represent sinus P waves. Slight variation in the P-P interval is the result of sinus arrhythmia.
• The first 4 beats represent a 4-beat run of fascicular NSVT. Dotted lines extending from these first 4 fascicular beats represent conduction back to the atria (resulting in the YELLOW arrow retrograde P waves).
• The different colored circles within the Atrial Tier — represent PACs arising from different sites within the atria.
• I've drawn the laddergram to reflect that I suspect each of the later 3 fascicular beats ( = beats #11,15,16) are fusion beats — though it is admittedly difficult to detect significant difference in QRS morphology between fascicular beats #15,16 vs QRS morphology of the pure fascicular beats #1-thru-4.

Figure-4: Laddergram illustration of today's rhythm.

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CASE Conclusion: Clinical Implications ...

There is no specific "classification" that fits all aspects of today's rhythm. The occurrence of so many PACs of different P wave morphologies brings to mind features of MAT (Multifocal Atrial Tachycardia) — but there are too many consecutive P waves of similar origin to be consistent with the concept of "true" MAT, in which P wave morphology and the PR interval varies from one-beat-to-the-next (ie, We see too many consecutive on-time RED arrow sinus P waves).

• PEARL #4: As discussed in ECG Blog #366 — Rather than strict definition of "MAT" — many patients manifest variations along the spectrum of MAT, in which there may be multiple P wave morphologies sandwiched between periods of fairly normal on-time sinus P wave activity. Such is the case in today's rhythm.
• 
  
• Clinically: Even when "pure" MAT is not present — rhythms with multiple PACs of multiple morphologies often "behave" in similar fashion to MAT in that: i) Severe pulmonary disease and/or "sick" patient with multisystem comorbidities (ie, acid-base and/or electrolyte abnormalities; shock; multi-system failure) are often the cause; and, ii) The BEST treatment is to "find and fix" the underlying cause (as per ECG Blog #366).
• As to the rest of the 12-lead ECG in today's case — supraventricular complexes (ie, beats #10,12,13 in leads V1,2 + beats #14 and 17 in leads V5,V6) — show increased voltage consistent with LVH — and ST-T wave changes consistent with LV "strain" — but this does not appear to be acute.
• 
  
• Finally: Today's rhythm further defies classification — because it includes frequent ventricular beats with a 4-beat run of fascicular NSVT.

MY Suggestion for Management:

Since today's patient is 92 and asymptomatic — We do not want to "do too much to him". Simply stated — "It is hard to make an asymptomatic patient feel better!"

• The above said — it is good to appreciate that even though today's arrhythmia does not fit the full definition of "MAT" — this rhythm does behave clinically in similar fashion as does MAT. Therefore — We should look for simple potentially "fixable" exacerbating factors, such as electrolyte imbalance (ie, Check serum K+ and Mg++ levels, as well as other electrolytes) — hypoxemia (Check O2 saturation levels) — heart failure, sleep apnea, dehydration, etc.
• If nothing "easily fixable" turns up abnormal — it may be that this 92-year old man has been in this rhythm for years! In that case — we may want to leave him alone.

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Acknowledgment: My appreciation to Chun-Hung Chen = 陳俊宏 (from Taichung City, Taiwan) 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.
• ECG Blog #185 — Reviews the Ps, Qs, 3R Approach to Rhythm Interpretation.
• ECG Blog #188 — Reviews how to read and draw Laddergrams (with LINKS to more than 80 laddergram cases — many with step-by-step sequential illustration).
• 
  
• ECG Blog #128 and ECG Blog #129 — on Fusion beats.
• 
  
• ECG Blog #366 — MAT explained.
• ECG Blog #199 — More on MAT.
• ECG Blog #65 — for an example of MAT in a patient with chronic pulmonary disease (plus more on the differential diagnosis of MAT).
• ECG Blog #200 — on Wandering Atrial Pacemaker.

I link to 2 additional 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 MAT:

• The January 5, 2020 post in Dr. Smith’s ECG Blog — for an example of MAT.
• The September 30, 2019 post in Dr. Smith’s ECG Blog — for an example of “MAT”, but without the tachycardia ...

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ADDENDUM (5/3/2024):

• Some additional information on MAT … 

ECG recognition of MAT (3:20 minutes Video).

 

Figure-3: Summary of KEY points related to MAT.