Saturday, January 21, 2023

ECG Blog #358 — A 20-Year Old with Bradycardia

The ECG in Figure-1 — was obtained from a previously healthy 20-year old man who presented with chest discomfort on inspiration — but no prior history of syncope/presyncope and no sign of heart failure.
  • No prior ECG had been done.
  • Other than a slow pulse — vital signs, oxygen saturation and physical exam were all normal.
  • Screening lab including complete blood count, thyroid function tests and serum electrolytes were unremarkable.

  • How would YOU interpret the ECG shown in Figure-1?
  • What is your diagnosis?
  • Does this patient need a pacemaker?

Figure-1: The initial ECG in today's case — obtained from a previously healthy 20-year old man who presented with chest discomfort on inspiration. How would you diagnose this tracing?

MY Initial Thoughts on Today's Case:
I found today's case intriguing for 2 reasons: i) The ECG diagnosis; and, ii) Clinical implications of the ECGs in today's case in view of the fact that they were obtained from a previously healthy 20-year old man.

The Initial ECG in Figure-1:
As always — I favor starting with the long lead II rhythm strip — and systematically assessing the Ps, Qs & 3Rs (See ECG Blog #185):
  • The ventricular rhythm in the long lead II rhythm strip of Figure-1 — is slow and fairly regular at a rate in the mid-40s.
  • The QRS is wide — with a QRS morphology consistent with LBBB (ie, all upright QRS in lateral leads I and V6 — and predominantly negative QRS in the anterior leads).
  • P waves are present! The PR interval before each of the 7 beats in this tracing is prolonged but constant (ie, at ~0.44 second). The finding of a constant PR interval in front of each beat tells us that there is conduction.
  • Two P waves are seen within each R-R interval. Considering the P-P interval that we see between these 2 P waves — this suggests that a 3rd P wave may be hiding within each of the QRS complexes. If so — this would suggest a fast and regular atrial rate of ~3 X 40-45/minute, or an atrial rate of ~130/minute.

Looking at the Rest of the 12-Lead:
As noted above — although the QRS is wide, all beats in Figure-1 appear to be conducted. QRS morphology is perfectly consistent with LBBB conduction.
  • QRS amplitude appears to be significantly increased (ie, with marked overlap of the huge S waves in anterior leads V2,V3). In an older adult — this would suggest LVH in addition to LBBB. However, the specificity of the finding of deep anterior S waves with LBBB is far less in younger adults (ie, today's patient is only 20).
  • T waves are peaked in multiple leads. These T waves are huge (ie, over 20 mm in height in leads V2,V3). Although this appearance would seem to suggest hyerpkalemia — this 20-year old man was previously healthy, and we are told that serum electrolytes were normal!

The RHYTHM: Putting It All Together
This initial ECG in today's case is extremely abnormal for a "previously-healthy" 20-year old man!
  • There is 2nd-degree AV Block — most probably with 3:1 AV conduction. The resultant ventricular rate is markedly bradycardic (ie, in the mid-40s).
  • The P waves that conduct do so with a markedly prolonged PR interval.
  • The QRS is wide — with morphology consistent with LBBB conduction.

  • BOTTOM Line: On the basis of this single initial ECG — one has to consider the diagnosis of Mobitz II 2nd-degree AV Block for ECG #1 (See ECG Blog #236for review of the 2nd-degree AV Blocks).

CASE Follow-Up:
A detailed work-up was undertaken in search of why this previously-healthy 20-year old man was now for the 1st time presenting for medical attention with the ECG shown in Figure-1:
  • Serum Troponins — negative.
  • Echo — was essentially normal (normal chamber size with ejection fraction ~55-60%).
  • Coronary CT — revealed a zero calcium score, without suggestion of coronary artery abnormalities.
  • Cardiac MRI — negative for fibrosis, scarring or edema.

  • Cardiac Stress Test — revealed chronotropic incompetence!

  • Autoimmune screening — negative.
  • Testing for Lyme Disease — negative.
  • Lamin A/C (LMNA) gene screen for mutations association with familial dilated cardiomyopathy — negative.


The Follow-Up ECG:
The tracing obtained after ECG #1 — is shown below in Figure-2. To facilitate comparison — I have put both of these tracings together.

  • What is the difference between these 2 tracings?
  • Is a pacemaker still needed?

Figure-2: To facilitate comparison — I've put the 2 ECGs in today's case together. What is the difference between these 2 tracings?

Comparison of ECG #1 and ECG #2:
There are several differences between these 2 tracings: 
  • The QRS complex has narrowed in ECG #2 (ie, LBBB conduction is no longer present!).
  • The ventricular rhythm is no longer regular in ECG #2. The overall ventricular rhythm is still slow (being faster in places than the ventricular rhythm in ECG #1 — but slower than in ECG #1 in other places).
  • The atrial rate has slowed compared to ECG #1.
  • The AV conduction ratio has improved (ie, it looks like there is now 2:1 AV conduction — compared to the 3:1 AV conduction ratio apparent in ECG #1).

  • Advanced POINT: The PR interval in ECG #2 remains constant and prolonged (ie, to ~0.44 second) before the QRS complex of beats #1-thru-5 and before beat #7. That said — careful measurement suggests that the PR interval before beat #6 has become slightly longer (ie, at ~0.48 second) than the other PR intervals in this tracing!

Looking Closer at Atrial Activity:
It's easier to appreciate what's happening with atrial activity in today's tracings — IF we add RED arrows over those P waves that we clearly see (Figure-3).
  • Not only has the atrial rate slowed in ECG #2 — but addition of the RED arrows in Figure-3 makes it much easier to appreciate that the P-P interval is now variable in this follow-up tracing. 

PEARL #1: As is evident for many of the examples of AV block that have appeared in this ECG Blog — it is extremely common for there to be a ventriculophasicsinus arrhythmia in association with 2nd or 3rd degree AV block. 
  • Much of the time (as is the case in Figure-3) — the shorter P-P interval is the one that “sandwiches” a QRS complex (the theory being that perfusion of the heart improves following ventricular contraction — with resultant shortening by a slight amount the P-P interval that contains a QRS).

Figure-3: I've added RED arrows over those P waves that we can clearly see in today's 2 tracings.

Atrial Activity in ECG #1:
For clarity in Figure-4 — I've separated the long lead II rhythm strip in ECG #1, from the rest of the 12-lead that appeared above it in Figure-3.
  • Doing so highlights how much more logical it seems that the underlying atrial rhythm in ECG #1 is Atrial Tachycardia (and that regular on-time P waves continue to occur where I've placed PINK arrows — at a rate of ~130/minute).

  • Advanced POINT: Further support that on-time atrial activity continues (ie, being hidden within each of the QRS complexes in Figure-4) — is suggested by the very subtle-but-real slight deformation of the terminal part of some QRS complexes by these hidden P waves (ie, the slight "extra" hump in the terminal part of the QRS that appears between the slanted BLUE lines for beats #4 and 5 — but which is not seen [GREEN lines] for some beats in which the end of the QRS is smooth).

Figure-4: I've added a number of PINK arrows to highlight how much more logical it seems that on-time atrial activity continues (hidden within each QRS complex) — throughout the entire long lead II rhythm strip in this tracing.

My Laddergram for ECG #2:
For clarity in Figure-5 — I've drawn a laddergram for the long lead II rhythm strip from ECG #2 that illustrates the following:
  • Group beating, albeit with slight variation in the atrial rate, as well as slight variation in the R-R intervals.
  • 2:1 AV conduction — in which the PR interval is markedly prolonged and constant (with the exception of slight additional lengthening before beat #6).

Figure-5: Laddergram for the rhythm in ECG #2.

KEY Points from Today's Case:
The unique aspect of today's case — is that this previously healthy 20-year old man only now presents with symptoms from a complex form of AV block that apparently had been present for some period of time. This leaves us with the following QUESTIONS to Answer:
  • Why was the QRS wide in ECG #1 — but not in ECG #2?
  • Why did the conduction ratio improve from 3:1 to 2:1 in the follow-up tracing that was done (as shown in the laddergram in Figure-5)?
  • How best to describe this patient's AV block?
  • Why was this patient without symptoms for so long?
  • Is a pacemaker needed?


PEARL #2: Rather than a fixed intraventricular conduction defect — the transient LBBB conduction that was seen in ECG #1 (but not in ECG #2) — may reflect a rate-related BBB (Bundle Branch Block).
  • As discussed in ECG Blog #242 — Conduction defects may sometimes appear as a result of an increase in heart rate. The interesting feature of this rate-related form of aberrant conduction — is that the rate of "onset" of BBB is not necessarily the same as the rate of "offset"
  • For example — Imagine a rhythm in which there is normal conduction (with a narrow QRS complex) for sinus rhythm at a rate of 70/minute — but, QRS widening occurs when the rate increases to 80/minute. Because the rate of "offset" is not necessarily the same as the rate of "onset" — it may be that the sinus rate needs to drop to as low as 50-60/minute before BBB conduction resolves.

  • This is relevant to today's case — since LBBB conduction appeared in the initial tracing — but not in any of the follow-up ECGs that were done while this patient was hospitalized. The diagnosis of Mobitz II with 3:1 AV Block was made on the basis of the high-grade block with QRS widening that was seen in ECG #1. A finding against the diagnosis of Mobitz II — would be the presence of a narrow QRS complex for conducted beats, as was seen in ECG #2 (and in all subsequent ECGs that were done on this patient).

  • NOTE: The fact that the QRS is narrow and the ventricular rate becomes slower in parts of ECG #2 — suggests that the reason for LBBB conduction in the initial tracing may have been rate-related. But because of the above noted discrepancy between the "rate of onset" and the rate of "offset" of rate-related BBB — it's impossible to prove this relationship with only the 2 tracings that are shown.
  • To Emphasize: Regardless of whether the LBBB conduction in ECG #1 is a reflection of rate-related BBB — development of BBB at a slow rate in the mid-40s is not a "normal" phenomenon in a 20-year old adult. That said, the diagnosis of Mobitz II would seem to be less certain in association with normal QRS duration.

PEARL #3: The reason for the improved AV conduction (from 3:1 in ECG #1 — to 2:1 in ECG #2)may simply be a result of a change in the atrial rate (and not the result of any change in the "severity" of AV conduction). This fundamental concept is all-too-often overlooked!
  • As noted above — the atrial rate in ECG #1 is ~130/minute.
  • The P-P interval becomes longer and irregular in ECG #2 — reflecting the ventriculophasic sinus arrhythmia of this 2nd-degree AV block. The atrial rate in this follow-up tracing varies from ~65-to-85/minute.

  • KEY Point: At the much slower atrial rate seen in ECG #2 — it may be that this patient's diseased AV node may be able to conduct more impulses (compared to the situation when the number of impulses arriving at the AV node is much higher). Therefore — Always take into account the relative atrial rate when assessing whether the "severity" of AV block may be increasing or decreasing.

PEARL #4: Rather than Mobitz II — I suspect the primary conduction defect in today's patient is a variation of AV Wenckebach (ie, of Mobitz I 2nd-degree AV block).
  • As emphasized in ECG Blog #236Mobitz I ( = AV Wenckebach) is by far the most common form of 2nd-degree AV block. In my experience — as many as 95% of all 2nd-degree AV blocks are Mobitz I. Clinically, the importance of recognizing when the Mobitz II form of 2nd-degree AV block is present — is that pacing is much more likely to be needed for this more severe form of block. 
  • KEY Point: When in doubt as to whether a patient with 2nd-degree AV block has a Mobitz I or Mobitz II defect — Statistics strongly favor Mobitz I.

  • ECG findings in today's case that further support the likelihood of a Mobitz I conduction defect include: i) The likelihood of rate-related BBB as the cause of QRS widening in the initial tracing; ii) The finding of marked 1st-degree AV block for all conducted beats (which is much more commonly seen in patients with Mobitz I than with Mobitz II); and, iii) The subtle-but-real increase in PR interval duration for the P wave before beat #6 in today's 2nd tracing.

PEARL #5: Some component of vagal tone may be operative in the rhythms seen in today's case. In support of this premise are the following: i) The patient is a previously healthy young adult male (Enhanced vagal tone would become even more likely if it turned out that today's patient performed regular endurance activities); ii) The PR interval is prolonged — and the PR interval is seen to increase for at least 1 of the conducted beats; and, iii) The sinus rate varies substantially in ECG #2.
  • The potential relevance of enhanced vagal tone in today's case — is related to the phenomenon of vagotonic AV Block, in which hard-to-predict variations in rate, PR intervals, and in the degree of AV block may sometimes be the sole result of increased vagal tone (See ECG Blog #61for illustration of this phenomenon)

PEARL #6: The KEY clinical question to answer in today's case — is whether a permanent pacemaker is indicated for this previously healthy 20-year old man?
  • The "shorter" answer to this question is YES — because: i) The patient is symptomatic; ii) Despite the thorough evaluation described above — no "fixable" cause of this patient's bradycardic 2nd-degree AV block was found; and, iii) There was chronotropic incompetence  on stress testing.

  • The "longer" answer to this question is more complex (See my discussion below regarding AV block in children and younger adults).

What is Chronotropic "Incompetence"?
Broadly defined — chronotropic incompetence is the inability to increase heart rate sufficiently to keep up with the increased demand of the patient's activities (Brubaker and Kitzman: Circulation 123:1010-1020, 2011).
  • Although I do not have access to specific stress testing results from today's patient — the report of "chronotropic incompetence" presumably entails the situation reflected above in Figure-4 — in which despite the increase in atrial rate — the reduced (3:1) ratio of AV conduction resulted in a clearly insufficient ventricular rate in the mid-40s.
  • Given the lack of a "fixable" cause of this patient's bradycardia — a permanent pacemaker was deemed necessary.


PEARL #7: As discussed in ECG Blog #307 — There are many potential causes of AV block. Although most commonly seen in adults in association with ischemic heart disease (ie, as the result of recent infarction) — or in older adults as the result of fibrosis or calcification of the atrioventricular conduction system — there are a variety of other Potential Causes of AV Block in children and adults (Figure-6)
  • Since some of the causes of AV block in Figure-6 may be treatable and/or resolve with time — a search for the cause is essential.
  • Given the young age of the patient in today's case — the KEY question was whether AV block was congenital, and only presenting for the 1st time at the age of 20.

Figure-6: Diagnostic considerations for a patient who presents in AV block (adapted from Mangi et al — StatPearls, 2021).

PEARL #8: The indications for permanent pacing are different in younger patients! Some patients function surprisingly well for long periods of time despite some degree of AV block. As a result — an "optimal balance" is sought between the immediate need for pacing vs the likelihood of pacer malfunction over time (with eventual need for pacer replacement).

Editorial NOTE: I found review of the literature on AV block in younger patients to be challenging — since there are still many facets of this entity that are uncertain. My summary below is based on review of the following references:


What is "Congenital" AV Block?
The overall incidence of CAVB (Congenital AtrioVentricular Block) is rare — occurring in ~1/20,000 live births. CAVB may occur in isolation — or it may be associated with conduction system abnormality that develops in association with one or more congenital cardiac malformations.
  • The term "congenital" AV block — is reserved for when the conduction defect is diagnosed: i) In utero; ii) At birth; or, iii) During the 1st month of life. 
  • I found it interesting that the way "congenital" AV block is diagnosed in utero — is by fetal echocardiography (ie, by assessing whether the normal sequential relationship exists between atrial and ventricular mechanical events — or is lacking, as it would be with complete AV block). After birth — the diagnosis is made by ECG.
  • NOTE: The literature I reviewed uses the abbreviation CCHB ( = Congenital Complete Heart Block). I've chosen to alter this to "CAVB" — to allow for cases of significant AV block that do not fit strict definition of "3rd-degree" (complete) AV block. 
  • At least anecdotally — many of the cases of AV block that I've encountered in younger adults do not manifest "complete" (ie, 3rd-degree) AV block. I take this as additional reflection of our suboptimal appreciation for the natural course of AV block that is presumably "congenital" — but which only presents in adulthood.
  • The entity of CAVB is not uniform — as there may be different etiologies. The 3 main etiologic groups are: i) CAVB with associated congenital cardiac defects; ii) CAVB as the result of maternal autoantibodies; and, iii) Idiopathic CAVB (which is by far the least common etiology).
  • Approximately 90% of patients have CAVB as a result of either associated congenital cardiac defects — or — as the result of maternal autoantibodies. The prognosis of those patients is significantly worse than the ~10% with idiopathic CAVB.
  • Idiopathic CAVB is a diagnosis of exclusion (ie, the patient has CAVB — but no congenital cardiac defects — and negative autoimmune antibodies). Whereas the first 2 categories are almost always diagnosed early (ie, in utero, at birth — or during the 1st month of life)Idiopathic CAVB may pass unnoticed until later in childhood or even adulthood — IF the ventricular escape rate is not overly slow, and the patient is relatively asymptomatic.

  • Physiologically — the reason patients with idiopathic CAVB may pass undetected until adulthood with no more than minimal symptoms — is that overall myocardial function may be adequate with the ability to increase the ventricular escape rate with activity (at least enough for the patient to function to the point that they do not realize their activity level is "less" than it should be).

  • Given a lack of documented cases with detailed follow-up — less is known about the course of patients who presumably have idiopathic CAVB. That said — the report by Li-Na Su et al is fascinating, since it details a specific case with 28 years of follow-up (!) — in which a patient with idiopathic complete AV block did not present until adulthood. Despite symptoms of recurrent syncope — the patient refused pacemaker implantation. Surprisingly, she did amazingly did well for many years (successfully completing an uneventful pregnancy — and participating in normal daily activities, including those with heavy exertion). This patient did well without pacing. She did not have any recurrence of symptoms over her extended follow-up period. 
  • CONCLUSION (based on this report by Li-Na Su): Patients with CAVB (including those with complete AV block) — do not make up a homogeneous group. Some such patients function surprisingly well, participating longterm in normal activities despite their severe conduction defect! Bottom Line: Previous "indications" for permanent pacing — need to be revisited on an ongoing basis, depending on specifics of the case at hand (as we continue to discover information regarding the "natural history" of different patients in the diverse group with CAVB).
  • Pacemaker implantation is not "risk-free" — especially when undertaken in patients at a very young age. Among potential complications that may develop over years of use are wire fracture; need for repeated battery replacement; infection; and pacemaker-induced heart failure, among others.

  • In contrast to patients with idiopathic CAVB — the course of patients with maternal autoantibodies as the etiology of their CAVB tends to be very different and more severe. Complete AV block may be seen in up to 5% of pregnancies in which the mother is positive with anti-Ro/SSA and/or anti-La/SSB antibodies — with a much higher rate of recurrence if the mother goes on to have additional pregnancies. Although these antibodies are most prevalent in mothers with autoimmune diseases (ie, rheumatoid arthritis, lupus, or other collagen vascular diseases) — a significant percentage of women may be asymptomatic carriers without any preexisting diagnosis of an autoimmune disorder. 
  • Presumably, the mechanism for developing CAVB — is immune-mediated injury of the conduction system as a result of transplacental passage of maternal autoantibodies.
  • Because of the very high infant mortality associated with autoimmune-related CAVB (which may attain ~15-30%)early pacing has generally been recommended.

  • In patients with CAVB as a result of congenital cardiac defects — longterm prognosis depends on the nature and severity of associated congenital heart disease, in addition to the severity of the AV block.

  • Overall, among the indications for permanent pacing of patients with CAVB are the following: i) Significant symptoms not due to a reversible cause; ii) Profound bradycardia with CAVB (even when symptoms are modest); iii) Associated left ventricular dysfunction (given high risk of developing dilated cardiomyopathy); iv) QRS widening; and/or, v) A very long QTc. In patients who are not immediately paced — regular follow-up to ensure that these indications do not subsequently develop is essential. 

Final CASE Follow-Up:
In today's patient — the above described negative work-up resulted in a presumed diagnosis of idiopathic CAVB that had gone undetected for the first 20 years of this patient's life. Because of chronotropic incompetence on stress testing — a permanent pacemaker was placed.

Acknowledgment: My appreciation to Mustafa Alalwan (from Abu Dhabi, UAE) for the case and this tracing. 

For MORE on Diagnosis of ABlocks/AV Dissociation:
  • ECG Blog #185 — Reviews the Ps, Qs, 3R Approach to Rhythm Intepretation.

  • ECG Blog #188 — for Review on How to Read (and DrawLaddergrams.

  • ECG Blog #307 — Reviews a case of an asymptomatic 40yo man who presented with bradycardia due to previously undetected AV Block.

  • ECG Blog #236 and ECG Blog # 237 — Reviews the 3 Types of 2nd-Degree AV Block (and how to define the term "high-grade" AV block).

  • ECG Blog #63 — Reviews a case of Mobitz I with Junctional Escape.
  • ECG Blog #186 — The AV Blocks (and when to suspect Mobitz I).
  • ECG Blog #191 — How to distinguish between AV Dissociation vs Complete AV Block.
  • ECG Blog #192 — The 3 Causes of AV Dissociation.

  • ECG Blog #242 — Review of Rate-Related BBB.

  • ECG Blog #61 — Review of Vagotonic AV Block.


  1. Amazing detective work in the tradition of the famed Sherlock Holmes! Methodical step by step and clue by clue interpretation augmented by Laddergram leads us to the diagnosis. Laddergram is not a lost art but thriving in this blog, thank you, Professor KG.

    1. Thank you! I LOVE laddergrams — they immediately explain what the interpreter is thinking — and help make this clear to anyone else interpreting the tracing — :)

  2. How can we interpret the normalization of T-wave under cLBBB in V4-6 & lead I-II before getting lab data(cardiac enzymes, electrolytes, etc)?

  3. Hello. I am sorry to say that I do not understand your question. There is only 1 LBBB tracing ... Lab work was normal. Could you please clarify what it is that you are asking? Thank you — :)

    1. Sorry, I didn't express clearly. I thought typical LBBB pattern in lateral leads was broad R wave with "ST-T depression". Therefore, I concerned the "positive T waves in V5-6& lead I in this case" might indicate myocardial injury change for LBBB; or positive T waves in V5-6 and lead I were normal for LBBB pattern? Thank you!

    2. Thank you Tony for clarifying your question. You are correct that the upright T waves with LBBB conduction is not typical for "secondary ST-T wave changes" seen with LBBB — which is part of the reason for the extensive work-up (which DID rule out acute infarction).