ECG Blog #420 — A "Fast" Complete Heart Block?

I was asked to interpret the 2-lead rhythm strip shown in Figure-1 — without the benefit of any history. What are YOUR thoughts?

• Is there AV block? If so — Is it complete AV block?

Figure-1: You are asked to interpret this 2-lead rhythm strip without the benefit of any history.

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NOTE: Today's rhythm is challenging — especially if you have not seen this type of rhythm before. That said, attention to the sequential PEARLS I present in my discussion below can greatly facilitate recognizing this rhythm within seconds the next time you encounter it!

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MY Thoughts on Today’s Rhythm: 

Assuming that today’s patient is not unstable hemodynamically (and does not require immediate synchronized cardioversion) — We can completely turn our attention to assessment of the rhythm. By the Ps, Qs & 3R Approach (which I review on ECG Blog #185):

• The Rate of the rhythm in Figure-1 is somewhat fast — averaging ~100/minute (ie, with an R-R interval close to 3 large boxes in duration for most of the tracing).
• The rhythm is clearly not Regular. The R-R interval is not the same throughout the tracing.
• It appears that there are at least some P waves, albeit P waves are not seen in all parts of this tracing.
• Although the QRS complex looks wider than it normally is — the QRS does not measure more than half a large box (ie, not more than 0.10 second) in either of the 2 monitoring leads shown in Figure-1. 

PEARL #1: Remember the saying, “12 leads are better than one”. The importance of determining whether the QRS complex of a tachycardia is wide or narrow — is that IF the QRS is narrow in all 12 leads, then the rhythm is supraventricular (and we have therefore ruled out the possibility of VT = Ventricular Tachycardia). The more monitoring leads we have available — the more accurate will be our determination about whether the QRS is wide or narrow.

PEARL #2: We only see 2 of the 12 leads of an ECG in Figure-1. This is important to appreciate — since sometimes a part of the QRS complex may lie on the baseline in one or more leads. When this happens — the QRS may “look” to be narrow in the lead(s) you are monitoring, whereas in reality the QRS is actually wide.

• It is for this reason that I always favor doing a 12-lead ECG as soon as this is feasible for any arrhythmia of uncertain etiology. Clinical management of the patient clearly differs if you can rule out the possibility of a ventricular rhythm. Unfortunately in today’s case — No 12-lead ECG was available.

Assessing the 5th Parameter:

Thus far — We’ve determined the following: 

• That the Rate of QRS complexes in today’s rhythm is fairly fast — but not quite Regular.
• That the rhythm is probably supraventricular (because the QRS is not more than half a large box in either of the 2 monitoring leads we are given)
• That at least some P waves are present.
• 
  
• The remaining parameter is the 3rd R — which  is determining IF any of the P waves in today’s rhythm are Related to neighboring QRS complexes. It turns out that this last parameter is KEY to solving today’s arrhythmia.

PEARL #3: The easiest way to assess for this 5th parameter — is to see if there are any PR intervals that repeat. And the BEST way to find any PR intervals that may be repeating — is to seek out any relative pauses in the rhythm — and to check out the PR interval before each beat that ends each pause.

• NOTE: The “pause” in the rhythm may be brief — and not much longer than the other R-R intervals. Figure-2 illustrates this principle — in which the R-R intervals between beats #4-5; 8-9; and 12-13 are slightly longer than other R-R intervals in today’s tracing.
• RED arrows highlight the P waves that precede each of the beats that end each of these short pauses. Isn’t the PR interval before beats #5, 9 and 13 equal?

PEARL #4: An important concept in “arrhythmia problem solving” — is based on the saying, “Birds of a Feather flock Together”. By this I mean that IF you see a certain ECG finding a number of times in a given tracing — then if you see a similar phenomenon that is not quite as precise — the chances are that you are seeing the same ECG finding!

• Take beat #1 in Figure-2 — which occurs at the very beginning of this tracing (which means that we do not know what came before beat #1). As a result, we can not know if beat #1 was preceded by a slight pause in the same way that beats #5, 9 and 13 are all preceded by a slight pause of the same duration. 
• BUT — Given the repetitive pattern of there being a slight pause after every 4th beat (ie, “Birds of a feather …” ) — and given that the PR interval preceding beat #1 ( = first RED arrow in Figure-2) is equal to the PR interval preceding beats #5,9,13 ( = the other RED arrows in Figure-2) — this is not by chance, and whatever relationship might be occurring between atrial activity and neighboring QRS complexes for beats #5-thru-16 — is almost certain to be the same phenomenon occurring for beats #1-thru-5! 

Figure-2: Applying the concept of “Looking for a slight pause in the rhythm” — I’ve labeled the 4 P waves that we clearly see with RED arrows. Note that the PR interval for these 4 P waves is the same!

PEARL #5: It’s time to determine IF there is an underlying regular atrial rhythm — which could be the case IF some P waves are hiding within certain ST-T waves. Figure-3 illustrates How to Look for “Hidden” P waves:

• Search the tracing looking for 2 P waves in a row that you can clearly see. RED arrows in Figure-3 illustrate 2 such P waves that are clearly seen in today’s rhythm.
• Using the P-P interval set by these 2 RED arrows locates the next spot to search for a “P wave in hiding”. Isn’t the T wave under the WHITE arrow in Figure-3 “fatter” than most other T waves in this tracing?
• The reason the T wave under the WHITE arrow is “fatter” — is that this is where the next consecutive P wave occurs.
• NOTE: Using calipers greatly facilitates the process. Using calipers instantly makes you “smarter” — and allows me to “solve” an arrhythmia such as today’s tracing within seconds that providers who do not use calipers are simply not able to solve.

Figure-3: How to find “hidden” P waves (See text).

Now that we have identified the P-P interval for 3 consecutive P waves (as shown by the 3 arrows in Figure-3) — it should take no more than seconds to “walk out” where the regularly-occurring P waves are located throughout the rest of today’s tracing (Figure-4):

Figure-4: RED arrows highlight where regular atrial activity is located throughout the rhythm in today’s case.

PEARL #6: Try to determine if the underlying atrial rhythm is a “sinus” rhythm — or an ectopic atrial rhythm. This determination is not always easy to make.

• A sinus rhythm — is defined by the presence of an upright P wave in lead II. This is because when limb lead electrodes are correctly placed — the direction of atrial depolarization as impulses arising from the SA node travel toward the AV node will be oriented close to +60 degrees in the frontal plane, which corresponds to the 60 degree electrical perspective of standard lead II in Einthoven’s Triangle.
• Therefore — IF P waves are not upright in lead II, then the rhythm is not sinus!
• The problem is that when P waves are upright in standard lead II (as they are in Figure-4) — then it may be difficult to distinguish between a sinus rhythm vs an ectopic atrial rhythm!

PEARL #7: Determining the atrial rate may help. In Figure-4 — the atrial rate is ~125/minute (which can be quickly estimated by the Every-Other-Beat Method reviewed in ECG Blog #210). 

• By the Every-Other-Beat Method — Given that the P-P interval of every-other-P-wave in Figure-4 is just under 5 large boxes in duration — this means that half the atrial rate is slightly faster than 300 ÷ 5 (ie, slight faster than 60/minute) — which means the actual atrial rate is ~125/minute.
• 
  
• The PEARL: The finding of a fast and regular atrial rate in association with an irregular supraventricular (narrow-QRS) rhythm — is much more likely to represent ATach (an ectopic Atrial Tachycardia) — than sinus tachycardia. The reason for this finding, is that Wenckebach conduction is commonly seen with ectopic ATach.

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Proving My Theory . . .

Using calipers — I was able to prove within seconds that my suspicion of ATach with Wenckebach conduction was the answer to today's rhythm.

• For clarity in Figure-5 — I've reproduced Figure-2, in which we see group beating (ie, beats #1-thru-4; #5-thru-8; #9-thru-12; #13-thru-16) — with each group separated by a slight pause of similar duration (ie, between beats #4-5; #8-9; #12-13) — with each pause ending with a conducted P wave (ie, the RED arrow P waves, each with an identical PR interval before beats #1,5,9,13). The repetitive pattern of these similarities can not be by chance!
• As soon as my calipers confirmed the underlying regular atrial rhythm (RED arrows in Figure-4) — I knew today's rhythm had to be ATach with Wenckebach conduction.

Figure-5: I've reproduced Figure-2 to highlight the repetitive pattern of "group beating" in today's rhythm (See text).

Knowing (from Figure-4) where each of the underlying regular P waves are located — allowed me to focus on the 2nd P wave in each group — which I've highlighted with PINK arrows in Figure-6. These PINK arrow P waves are each conducting the 2nd QRS complex in each group of beats (ie, PINK arrow P waves are conducting beats #2,6,10 and 14).

• Note that the PR interval of each PINK arrow P wave is longer than the PR interval before the 1st beat in each group (highlighted by each RED arrow P wave).

Figure-6: I've highlighted the 2nd P wave in each group with a PINK arrow.

Next, in Figure-7 — I focused on the 3rd and 4th P waves in each group (highlighted by light and dark BLUE arrows, respectively).

• Note progressive lengthening of the PR interval for each of the colored arrows in each of the 4 groups!

Figure-7: I've highlighted the 3rd and 4th P waves in each group with light and dark BLUE arrows, respectively

Finally, in Figure-8 — I highlight with YELLOW arrows, the location of the next on-time P wave.

• It is these "on-time" YELLOW arrow P waves that represent the dropped (non-conducted) P wave in each of the Wenckebach cycles in today's rhythm.
• This is as it should be with Wenckebach conduction — in that these non-conducted YELLOW P waves occur at the beginning of the slight pause between each group — after which the following on-time P wave (ie, the next RED arrow P wave) begins a new cycle with a shorter PR interval.

Figure-8: YELLOW arrows highlight the non-conducted P wave in each group — after which the next Wenckebach cycle begins.

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The Laddergram . . .

The above derivation for today's rhythm is rendered easier to see in Figure-9 by use of laddergram illustration.

• For clarity in Figure-9 — I've kept the coloration of arrows from Figure-8, to facilitate appreciation of progressive lengthening of each PR interval within each of the groups — until the 5th P wave in each group ( = the YELLOW arrow P waves) are non-conducted — followed at the end of each short pause, by resumption of conduction with PR interval shortening for the 1st beat in the next group (highlighted by each RED arrow P wave).

Figure-9: Laddergram illustration of today's rhythm.

Figure-10 is what today's laddergram looks like without coloration.

Figure-10: Final laddergram.

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FINAL Thoughts on Today's Rhythm:

As per my Note at the beginning of today's case — today's rhythm is a challenging one if you have not seen this entity before. But once you are aware of this arrhythmia presentation — it becomes EASY to recognize within seconds of seeing the tracing.

• Repetitive patterns are unlikely to be due to chance! Cement this concept in your mind by going back to the original tracing (which is why I once again show Figure-1 below, without any P waves labeled).
• 
  
• As you now take another LOOK at this initial tracing — Isn't it now easier to appreciate group beating with a repetitive pattern of similar intervals — in which each of the short pauses are terminated by easily-identifiable P waves with the same PR interval before beats #1,5,9 and 13?
• IF you used calipers to facilitate recognizing these relationships — Wasn't it EASY to establish within seconds these similarities in intervals?
• 
  
• BOTTOM Line: Once you recognize that today's rhythm is supraventricular — with group beating — and with fast, regularly-occurring P waves — that show clear conduction of the 1st P wave at the end of each pause — you have essentially established that the rhythm is ATach with Wenckebach conduction.
• Today's rhythm is not complete AV block — because complete ( = 3rd-degree) AV block is most often associated with a regular escape rhythm — and the ventricular rhythm in Figure-1 is clearly not regular!
• The "good news" — is that most of the time when ATach is associated with the group beating pattern of 2nd-degree AV Wenckebach — the conduction defect usually resolves once the ATach is controlled.

Figure-1: Take another LOOK at today's rhythm!

 

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Acknowledgment: My appreciation for the case and this tracing that was anonymously sent to me for my opinion.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #185 — reviews the Ps, Qs & 3R Approach (Listen to Audio Pearl #3 in this post).
• ECG Blog #188 — Reviews how to read and draw Laddergrams (with LINKS to more than 90 laddergram cases — many with step-by-step sequential illustration).
• ECG Blog #267 — Reviews with step-by-step laddergrams, the derivation of a case of Mobitz I with more than a single possible explanation.
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• ECG Blog #210 — for review of the Every-Other-Beat Method for rapid estimation of heart rate (See Video Pearl #27 in this post).
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• ECG Blog #229 — reviews distinction between AFlutter vs ATach.
• The November 12, 2019 post in Dr. Smith's ECG Blog — in which I review my approach to a Regular SVT rhythm.

• ECG Blog #261 and ECG Blog #370 — for additional examples of ATach with Wenckebach conduction.
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• ECG Blog #192 — The 3 Causes of AV Dissociation.
• ECG Blog #191 — Reviews the difference between AV Dissociation vs Complete AV Block.
• ECG Blog #389 — ECG Blog #373 — and ECG Blog #344 — for review of some cases that illustrate "AV block problem-solving".

ECG Blog #419 — The Cause of ECG #1?

I was sent the 2 ECGs shown in Figure-1 — which were recorded from an elderly man whose heart beat "has been irregular for years". No clear history for recent chest pain — but the patient "has not been well" for the previous week. Regarding the 2 ECGs in Figure-1: 

• ECG #1 is the initial tracing obtained at the scene by the EMS (Emergency Medical Systems) team — in association with an alert but markedly hypotensive patient.
• ECG #2 was recorded a short while after ECG #1 by the EMS team — but before any treatment other than ASA was given. As might be imagined — the patient suddenly "felt much better".

QUESTIONS:

• How would YOU interpret these 2 ECGs?
•   — How might ECG #2 be related to ECG #1?

Figure-1: The 2 ECGs in today's case. (To improve visualization — I've digitized the original ECG using PMcardio). 

MY Thoughts on the 2 ECGs in Figure-1:

Even without a long lead rhythm strip — it is easy to understand why today's patient was markedly hypotensive in association with ECG #1.

• Atrial activity is present in ECG #1 — in the form of seemingly regular upright P waves in each of the inferior leads — at a regular rate of ~115/minute. 
• I suspect that none of the P waves in ECG #1 are conducted.
• Detection of atrial activity is much more difficult in the chest leads due to a large amount of baseline artifact — although evidence of atrial activity at a similar rate is seen toward the end of lead V1.
• The above said — intermittent ventricular complexes of varying morphologies are seen (albeit with much distortion from artifact).
• The longest pause occurs in simultaneously-recorded leads aVR,aVL,aVF — with no ventricular complex seen after the 1st beat in these leads until the lead change to V1,V2,V3 occurs (ie, almost 12 large boxes = 2.4 seconds later). We have no idea how long the pause was before the 1st beat in ECG #1 was recorded.
• 
  
• Clinical IMPRESSION: I would interpret ECG #1 as suggestive of near ventricular standstill — with underlying atrial tachycardia, extended pauses, and no reliable ventricular escape focus. This is often a pre-lethal rhythm.
• 
  
• PEARL #1: The rhythm in ECG #1 is more than just "complete AV block". This is because in addition to no conduction of any of the sinus P waves — the presence of a fairly regular escape pacemaker that is usually seen with complete AV block is absent. Instead, we see extended pauses that are intermittently interrupted by irregular (and unreliable) ventricular complexes arising from different ventricular sites.

Before any treatment — ECG #2 was recorded:

• Normal sinus rhythm has spontaneously returned! Interestingly — the rate (and morphology) of sinus P waves is virtually unchanged with respect to the unconducted P waves that were seen in ECG #1, the difference being that there is now 1:1 conduction of sinus impulses with a normal PR interval!

NOTE: The QRS complex of conducted beats in ECG #2 is wide. QRS morphology is interesting in that it resembles RBBB (Right Bundle Branch Block) conduction in the chest leads — but LBBB (Left Bundle Branch Block) conduction with marked left axis in the limb leads. 

• The tall R wave (qR morphology) in lead V1 of ECG #2 — in association with a fairly wide terminal S wave in lead V6 — suggests RBBB conduction.
• The predominantly upright widened QRS complexes in leads I and aVL of ECG #2 — suggests LBBB conduction — with the predominantly negative QRS complexes in each of the inferior leads indicative of marked LAD (Left Axis Deviation).

PEARL #2: As described in ECG Blog #394 — QRS widening in the presence of sinus rhythm, in which QRS morphology is consistent with RBBB conduction in the chest leads — but LBBB conduction in the limb leads (especially with a leftward axis) — suggests the entity known as MBBB (Masquerading Bundle Branch Block). This is precisely the picture of the QRS morphology that we see in ECG #2.

• I review my user-friendly approach to the ECG diagnosis of the Bundle Branch Blocks in ECG Blog #282 — and to Hemiblocks and Bifascicular Blocks in ECG Blog #203. In brief — the 3 KEY leads that allow accurate diagnosis of RBBB and LBBB within seconds (!) — are right-sided lead V1 and left-sided leads I and V6.
• Supraventricular conduction defects not consistent with either RBBB or LBBB in all 3 of these key leads are most easily classified as IVCD (IntraVentricular Conduction Defect) — with this category representing the "end result" of a number of different pathophysiologic processes.
• 
  
• MBBB is a special type of IVCD that although uncommon, is important to recognize because it identifies a group of patients with: i) Very severe underlying heart disease; ii) A much higher predisposition for developing complete AV block (and needing a pacemaker); and, iii) An extremely poor longterm prognosis.
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• NOTE: Variations on this above "theme" of MBBB are common. Thus, the S wave that is typically associated with RBBB patterns in lateral chest leads V5,V6 may or may not be present. In the limb leads, rather than a strict LBBB pattern — more of an extreme LAHB (Left Anterior HemiBlock) pattern may be seen (ie, with wide and predominantly [if not totally] negative QRS complexes in the inferior leads — and with a smaller [blunted] terminal s wave in leads I and aVL).

PEARL #3: Knowing the clinical history may aid in recognition of IVCD patterns that are consistent with MBBB (ie, if the patient has a known history of severe, underlying heart disease). 

• Distinction from simple bifascicular block (ie, with RBBB/LAHB) — may be facilitated by seeing one or more of the following: i) More of a monomorphic upright QRS in lead V1 (which lacks the neatly defined, triphasic rsR' with taller right "rabbit ear" seen with typical RBBB); ii) Lack of a wide terminal S wave in lateral chest lead V6; iii) Seeing an all-positive (or at least predominantly positive) widened QRS in leads I and/or aVL, with no more than a tiny, narrow s wave in these leads; and/or, iv) Seeing widened, all-negative (or almost all-negative) QRS complexes in the inferior leads.

What About Today's ECGs?

Although details of the history of today's patient are lacking — the patient is elderly — he has had "an irregular heart beat for years" — and his initial ECG on EMS arrival ( = ECG #1) clearly suggests advanced conduction system disease with a potentially lethal rhythm were it not for spontaneous conversion to the tracing shown in ECG #2.

• In this clinical context — findings in ECG #2 are clearly consistent with masquerading BBB. 
• 
  
• A permanent pacemaker is needed. 

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Acknowledgment: My appreciation to Max-Gordon-Hall (from Batlow, New South Wales, Australia) 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 #282 — reviews 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.
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• ECG Blog #394 — reviews another case of Masquerading BBB.

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ADDENDUM #1 (3/6/2024): 

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In follow-up to the Comment I have just received from H.S.Cho — I would expand on my description of the cardiac rhythm in ECG #1 from today's case.

• Given the history in today's case (ie, Sudden onset of the rhythm seen in ECG #1 — that within a minute spontaneously resolved) — Rather than "near ventricular standstill" — this rhythm is best described as PD-PAVB (Pause-Dependent Paroxysmal AtrioVentricular Block).
• 
  
• For clarity — I have reproduced Figure-1 from today's case.

Figure-1: The 2 ECGs in today's case. 

Paroxysmal AtrioVentricular Block (PAVB):

As described by Bansal et al (J Arrhythmia 35:870-872, 2019) — Bosah et al (Cureus 14[7]: e27092, 2022) — and Uhm et al (Heart Rhythm Case Rep 4(5):197-199, 2018) — the entity known as PAVB is a potential cause of syncope that is easily overlooked and which is potentially lethal (probably more often than is commonly realized).

• PAVB is characterized by the sudden, unexpected onset of complete AV block with delayed ventricular escape — therefore resulting in a prolonged period without any QRS on ECG. Prior to the prolonged pause — the patient manifests 1:1 AV conduction without other evidence of AV block (which is why onset of PAVB is typically so unsuspected!).
• Because of its totally unexpected onset and propensity to result in sudden death — PAVB is difficult to document and significantly underdiagnosed.
• Three mechanisms for producing PAVB have been described: i) Vagally mediated (ie, Vagotonic Block — as described in ECG Blog #61, with the references listed at the end this Blog post citing instances of transient asystole from excessive vagal tone!); ii) Intrinsic (Phase 4 = pause- or bradycardic-dependent) PAVB; — and, iii) Idiopathic.

i) Vagotonic AV Block:

This form of PAVB is potentially benign when it results from a transient profound surge of parasympathetic tone in an otherwise healthy individual (as might occur with an episode of severe vomiting; a fit of severe coughing; vasovagal reaction from a blood draw).

• The problem with vagotonic PAVB is localized to within the AV Node.
• There will often be a "prodome" of diaphoresis, nausea, dizziness — with the patient aware of imminent fainting.
• 
  
• Characteristic ECG findings of vagotonic PAVB include progressive sinus rate slowing — often associated with an increasing PR interval and a narrow-QRS escape focus — followed by recovery with progressive return to a normal sinus rate and normal PR interval.

ii) Intrinsic PAVB:

Several names have been attached to this mechanism of PAVB — including most commonly "Phase 4 AV block" and/or PD-PAVB (Pause-Dependent Paroxysmal AtrioVentricular Block).

• PD-PAVB is the most likely mechanism for the cardiac rhythm in ECG #1 from today's case. The underlying pathology is severe His-Purkinje System disease (strongly suggested by the presence of MBBB in ECG #2 of today's case). This form of PD-PAVB is likely to be fatal unless the patient receives a permanent pacemaker.
• The interesting pathophysiology of PD-PAVB results from chance occurrence of an "appropriately-timed" PAC or PVC that partially depolarizes the diseased HPS (His-Purkinje System) at a specific point in the cycle that renders the poorly-functioning HPS unable to complete depolarization. The resultant prolonged pause in ventricular depolarization may only resolve if another "appropriately-timed" PAC or PVC occurs at the precise point needed to "reset" the HPS depolarization cycle (which presumably explains why the patient in today's case spontaneously recovered).
• Of note — although severe underlying HPS disease is evident from the MBBB seen in ECG #1 of today's case — up to 1/3 of patients with PD-PAVB do not show evidence of conduction defects on ECG, thereby complicating documentation of this diagnosis.
• 
  
• PEARL #4: In addition to seeing MBBB in ECG #2 — the fact that the atrial rate remains the same in both ECG #1 and ECG #2 is yet one more reason why the rhythm in ECG #1 does not represent simple vagotonic PAVB.

iii) Idiopathic PAVB: 

This is the most recently described form of PAVB — in which findings are not consistent with either of the other 2 forms.

• The baseline ECG before idiopathic PAVB tends to be normal.
• No "trigger" for PAVB is evident (ie, no source of excessive vagal tone — and no precipitating PACs/PVCs are seen).

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NOTE: The conduction disturbance shown in ECG #1 from today's case differs from that shown in ECG Blog #342 — in which the initial rhythm was AFib (ie, no P waves present for the first 6 beats in this tracing) — followed by a prolonged flat line pause (nearly 5 seconds in duration) — until finally a QRS complex preceded by a P wave (that may or may not have been conducting) was seen.

• Whether the prolonged flat line pause in this Blog #342 example represents another variation of PD-PAVB due to severe underlying disease of the His-Purkinje System — or reflects severe SA Node disease (ie, Sick Sinus Syndrome) — or most likely represents some combination of the two, is uncertain from the single ECG I was provided with.
• That said — the BOTTOM Line remains the same, namely that assuming nothing "fixable" is found — permanent pacing will be needed.

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ADDENDUM #2 (9/1/2025): 

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My credit to WB Ren for his comment in the EKG Club that has made me rethink about the fascinating electrophysiology of the heart's conduction system.

• WB Ren's comment relates to the phenomenon of changing P wave morphology, that rather than being due to a wandering atrial pacemaker shift in the atrial site of impulse formation — may at times result from a phenomenon similar to that seen in today's case (ie, instead of a diseased AV node or Purkinje conduction system — the problem may be Phase-4 Block in some but not all portions of the SA node — thereby resulting in an intermittent change in P wave morphology).
• For the basics of Phase-4 Block (Bradycardia-dependent Block) — I found this explanation in the on-line ECGbook enlightening.
• Additional examples and explanation of Phase-4 Purkinje System Block can be found in the Ulm et al manuscript HeartRhythm Case Rep 4(5):197-199, 2018.
• 
  
• With the concepts illustrated by my above link to the on-line ECG book — I found the stepwise AI explanation of the physiology of Phase-4 Block much more understandable than it previously had been to me. I've therefore copied below this AI explanation.

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ECG Blog #418 — A Single Lead Tells the Tale ...

The ECG in Figure-1 was obtained from a previously healthy man in his 40s — who presented to the ED (Emergency Department) with new-onset CP (Chest Pain) that awakened him from sleep.

• ECG #1 was recorded ~90 minutes after the patient was awakened from sleep. He was still having CP. 

QUESTIONS:

• In view of this history — How would YOU interpret the ECG in Figure-1?
• Does a single lead “tell the tale”?

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

MY Thoughts on the ECG in Figure-1:

The important points about today’s history are: i) That the patient is a previously healthy man in his 40s; — ii) That the patient was awakened from sleep by new CP; — and, iii) That his CP was still ongoing 90 minutes after it began, at the time ECG #1 was recorded in the ED.

• The ECG in Figure-1 shows normal sinus rhythm at ~75/minute — with normal intervals (PR-QRS-QTc) and axis — and no chamber enlargement.

Regarding Q-R-S-T Changes:

• Q waves: There are no Q waves. There is a small-but-present initial positive deflection ( = r wave) in lead III (I don't count as "Q waves" the initial negative deflections we see in leads aVR and V1 — since it is normal to see Q waves in these leads).
• R wave progression: There are good-sized R waves beginning in lead V2 — albeit there is slight delay in transition (with the R wave becoming taller than the S wave is deep only between leads V4-to-V5).

What About ST-T Wave Changes?

As we assess today's initial ECG for ST-T wave changes — It is important to remember that this patient was previously healthy — and — he was awakened from sleep by CP that was still present 90 minutes later (ie, at the time this initial ECG was recorded!).

• As a result — We need to consider this patient to be in a higher-risk group for having an acute event. This point emphasizes that the burden of proof falls on us as medical providers to prove that this patient is not having an acute event, rather than the other way around!

We Need to Remember the Following:

• Even with an acute event — the initial ECG may not necessarily show remarkable changes — and/or — ECG changes may be present, but subtle (and sometimes only recognized when compared to a prior baseline ECG on the patient — or when compared with serial ECG changes over time). 
• PEARL #1: Even with an ongoing, extensive acute MI — the initial high-sensitivity troponin may sometimes be normal.
• 
  
• PEARL #2: It is important to note and correlate the presence and relative severity of symptoms with each serial ECG that is done. This is because the course of an acute OMI ( = an acute MI that results from acute coronary Occlusion) — is not always predictable. Instead, even before treatment — there may be spontaneous reopening of the "culprit" vessel — which often can be recognized by reduced CP that occurs in association with improved ECG changes.
• Spontaneous reopening of the "culprit" vessel may result in "pseudo-normalization" of ECG changes (IF the ECG is recorded "between" the stage of acute ST elevation — and the later stage of coronary reperfusion as ST elevation evolves into ST depression and T wave inversion). 
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• KEY Clinical Point: This "pseudo-normalization" stage still mandates prompt cath with PCI, because what spontaneously reopens — may just as easily reocclude at any point in time if not prevented by PCI.

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CHALLENGE:

With the above caveats in mind — Take Another LOOK at today's initial ECG in Figure-1:

• Which single lead in ECG #1 tells the tale? 

ANSWER (shown below):

I highlight the answer to the above "Challenge Question" in Figure-2:

Figure-2: I highlight the KEY lead in today's initial ECG.

 

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Regarding ST-T Wave Changes in Figure-2:

As per the title of today's ECG Blog — one KEY lead "tells the tale".

• ST-T wave changes in the limb leads show nonspecific ST-T wave flattening — but nothing that looks acute.
• I've highlighted within the RED rectangle in Figure-2 the single lead ( = lead V3) that in a patient with new severe CP is clearly abnormal. While a slightly elevated, gently upsloping ST segment is common and normal in leads V2,V3 — there is definite straightening of the ST segment in this lead on the initial ECG — and the amount of ST elevation (seen with respect to the dotted RED line in this V3 lead) is excessive. This represents a hyperacute ST-T wave in lead V3 until proven otherwise! 

PEARL #3: To emphasize that lead V3 is the KEY lead in today’s initial ECG — without which I would not have diagnosed acute OMI. But since we know (for the reasons stated above) that in a patient with new CP, that the ST-T wave in lead V3 is hyperacute — I also interpreted the 2 neighboring leads in Figure-2 ( = leads V2 and V4) as abnormal and consistent with acute LAD OMI until proven otherwise:

• Lead V2 — The amount of ST elevation in lead V2 is not necessarily excessive, given how common slight ST elevation is normally seen in anterior leads V2,V3. But in the context of lead V3 definitely showing a hyperacute ST-T wave — I thought there was a bit more “straightening” of the initial part of the ST segment in lead V2 that I would normally expect (at least in the 1st complex in this lead).
• Lead V4 — While not necessarily abnormal if looked at as an isolated finding — I thought the amount of ST elevation in neighboring lead V4 to be a bit more than is usually expected in this lead. And, at least for the middle complex in this lead — there seemed to be a bit more-than-expected ST segment straightening.
• 
  
• To EMPHASIZE: If not for lead V3 — I would not have interpreted leads V2 and V4 as necessarily abnormal. This is especially true in view of: i) The surprisingly good R wave progression that we see in ECG #1 — with an R wave of already 7-8 mm by lead V2 (whereas there is commonly “loss of R wave” in anterior leads with acute LAD OMI); and, ii) The complete lack of abnormality in the remaining chest leads ( = leads V1,V5,V6). It is lead V3 that "tells the tale"!

PEARL #4: As stated earlier — an initial ECG will not always be diagnostic. The KEY is to appreciate that in most patients — the process of an acutely evolving coronary occlusion is dynamic — sometimes showing dramatic changes in as short a period as between 5-10 minutes (See ECG Blog 115 for a case in which such dramatic ST-T wave changes occurred in just 8 minutes!).

• The “Take-Home” Message from today's case is clear — IF you are at all uncertain about whether your patient with CP is or is not acutely evolving an OMI — Repeat the ECG soon and often — until you can confidently answer this question!

Today's CASE Continues: 

Given any uncertainty you might have as to whether today's patient was evolving an acute OMI — the initial ECG should have been repeated within 15-20 minutes.

• The ECG was only repeated 80 minutes later. To facilitate comparison in Figure-3 — I have put these first 2 ECGs together. What do YOU see?

Figure-3: To facilitate comparison — I've put the first 2 tracings in today's case together. What has changed? (To improve visualization — I've digitized the original ECG using PMcardio).

Comparison between ECG #1 and ECG #2:

The BEST way to compare serial ECGs — is to put them side-by-side, as I have done in Figure-3.

• Given our concern regarding lead V3 in ECG #1 — I began assessment of ECG #2 by looking at this lead, and at its neighboring leads.
• Compared to ECG #1 — there is now unmistakeable straightening of the ST segment takeoff in lead V3 of ECG #2, with reduced T wave amplitude.
• Lead V4 in ECG #2 — is now unmistakeably elevated (with straightened ST segment takeoff).
• Each of the remaining chest leads also show differences. There is subtle-but-real ST elevation now in leads V1, V2 and V5 — and some ST depression in lead V6 than was not previously present. 
• 
  
• Limb lead changes in ECG #2 are subtle — but in the context of the above noted chest lead changes, I believe the slightly increased inferior lead T wave amplitude and ST-T wave flattening in lead aVL is real.
• 
  
• PEARL #5: Did YOU Notice the loss of R wave amplitude in ECG #2? There is now a QS pattern in lead V2, with noticeably reduced R wave amplitude in leads V2-thru-V5 compared to ECG #1. 

BOTTOM Line: If there was doubt about the diagnosis from ECG #1 — the repeat ECG in Figure-3 is now clearly diagnostic of acute LAD OMI because: i) Dynamic ST-T wave changes are seen in virtually all leads compared to the initial tracing — including progressive ST elevation in leads V2-thru-V5; and, ii) Loss of R wave amplitude in these chest leads.

• The Important LESSON: Given the history of new-onset severe CP — acute LAD OMI can be diagnosed (or at least strongly suspected) from the initial ECG in today's case. But even if there was uncertainty about ECG #1 — definitive diagnosis could have been made much sooner by repeating this initial tracing within 10-15 minutes (instead of waiting 80 minutes).

CASE Conclusion: 

The diagnosis of acute LAD OMI was made once the repeat ECG in Figure-3 was obtained. Given unavailability of cardiac catheterization — Streptokinase was administered.

• ECG #3 was recorded after completion of Streptokinase infusion — in association with clinical improvement. What do YOU see?

Figure-4: Comparison of ECG #2 — with ECG #3, recorded after completion of Streptokinase. (To improve visualization — I've digitized the original ECG using PMcardio).

 

Regarding the Post-Streptokinase ECG in Figure-3:

Streptokinase infusion was effective!

• Other than slight residual ST elevation in leads V1,V2 — ST elevation in other chest leads has essentially resolved!
• Although there has been loss of R wave amplitude compared to the initial ECG — there has been no further loss of R wave amplitude since ECG #2.
• There is now terminal T wave inversion — that begins in lead V2, and extends through to lead V6. In association with clinical improvement of this patient — ECG #3 now shows reperfusion T waves consistent with effective thrombolytic infusion.

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Acknowledgment: My appreciation to Kianseng Ng (from Malaysia) 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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• 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.
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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).