Thursday, May 16, 2024

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.

  • 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 IschemiaSee 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. 


Acknowledgment: My appreciation to Mayan Kain (from Tel Aviv, Israel) for the case and this tracing.




Related ECG Blog Posts to Today’s Case:

  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.

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

    • 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.

    • ECG Blog #337 — A "NSTEMI" that was really an ongoing OMI of uncertain duration (presenting with inferior lead reperfusion T waves).

    • 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).

    • ECG Blog #203 — reviews ECG diagnosis of Axis, Hemiblocks and Bifascicular Blocks.


    Saturday, May 11, 2024

    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.

    • 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.

    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 ... 


    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.

    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?

    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.


    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.

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

     Related ECG Blog Posts to Today’s Case: 

    • ECG Blog #185 — Reviews the Ps, Qs and 3R Approach to Systematic Rhythm Interpretation.

    • ECG Blog #232 — Reviews the causes of Bigeminy.

    • ECG Blog #164 — Reviews a case of Mobitz I 2nd-Degree AV Block, with detailed discussion of the "Footprints" of Wenckebach.
    • ECG Blog #252for a similar case as today (with LINKS to more examples of blocked PACs).



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


    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. 


    • 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).


    Saturday, May 4, 2024

    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. 

    • 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).

    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.


    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.

    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.

    • 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 #1,2,3,4beat #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).

    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.


    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 asymptomaticWe 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.

    Acknowledgment: My appreciation to Chun-Hung Chen = 陳俊宏 (from Taichung City, Taiwan) for the case and this tracing.

    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 #366MAT 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 ...


    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.