ECG Blog #534 — What is or is not Conducting?

I was sent this ECG with the question, "What is or is not conducting?" Unfortunately — no clinical information was available. 

QUESTIONS:

• What is the rhythm?
• There are multiple interesting ECG findings on this tracing with regard both to the rhythm, as well as to the 12-lead ECG. How many of these findings can you identify?
• Do you need to draw a laddergram in order to interpret this tracing?
• Is there complete AV block?

Figure-1: Today's ECG that was sent to me. (To improve visualization — I've digitized the original ECG using PMcardio).

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NOTE: This is an extremely challenging ECG. Regardless of how far you got with your interpretation — there is much to learn for providers of all experience levels.

• Confession: My initial impression for the rhythm was wrong.
• PEARL #1: I can figure out 90-95% of complex rhythms within seconds without the need to draw a laddergram. That said — it's important to appreciate that there will always be some rhythms for which even arrhythmia specialists may not be able to determine a precise etiology without aid of a laddergram. Today's case is one of those rhythms.
• That said — You do not need a laddergram in today's case in order to make a time-efficient diagnosis of the essentials needed for appropriate initial management. As a result — I divide my discussion into 2 Parts: i) Detailed discussion of multiple interesting findings in today's ECG (including my proposed laddergram for the etiology of the rhythm); — and, ii) The steps I used to expedite time-efficient assessment sufficient for appropriate clinical decision-making.

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Part 1: Details of the many Interesting Findings:

As always, I like to start with assessment of the rhythm — for which I favor the Ps, Q's, 3R Approach for optimal time-efficient rhythm interpretation (See ECG Blog #185 — for review of the Ps,Qs,3Rs).

• NOTE: It does not matter in what sequence we assess the Ps, Qs and 3Rs. As a result — I do not always look first for P waves. Instead — I often start with whichever of the 5 KEY parameters is easiest to assess.
• Focusing on the long lead II rhythm strip at the bottom of the tracing — We should be able to appreciate that the rhythm is not Regular. But because of the relatively small difference between R-R intervals — it could be easy to mistake this tracing for a regular rhythm. Instead, there is a regular irregularity to the rhythm ( = group beating in the form of alternating longer-then-shorter R-R intervals).

PEARL #2: Use of calipers is essential for interpretation of complex rhythms such as this one. The simple fact is that with minimal practice — Use of calipers greatly speeds up and increases the accuracy of your interpretation.

• In Figure-1 — Longer R-R intervals ( = R-R intervals between beats #1-2; 3-4; 5-6; and 7-8) — alternate with shorter R-R intervals ( = R-R intervals between beats #2-3; 4-5; and 6-7).
• PEARL #3: Practically speaking — this finding of alternating longer-then-shorter R-R intervals is too consistent in Figure-1 to be due to chance. This means there is "group" beating — which should always suggest the possibility of some form of Wenckebach conduction (ie, There are other causes of group beating not due to Wenckebach, such as atrial bigeminy with either blocked or conducted PACs. That said — it is helpful clinically to always consider Wenckebach conduction whenever you realize that there is a repetitive pattern of beats).

Continuing with the Ps, Qs and 3Rs ... 

• The QRS in Figure-1 is intermittently wide. Depending on which lead(s) you used to assess QRS width — it could be EASY to overlook the fact that some QRS complexes are wide, while others are not wide.
• PEARL #4: 12 leads are better than one! Appreciation that some QRS complexes are wide while others are not is best seen in lead V1 — in which beat #5 (which corresponds to the 1st beat seen in lead V1) is wide with  the appearance of RBBB conduction. On the other hand — beat #6 ( = the 2nd beat in lead V1) is narrow! (See Figure-2).
• Armed with the knowledge that beat #5 in Figure-2 is wide, but beat #6 is not wide — We can see that in the long lead II rhythm strip, a terminal S wave is present at the end of every-other-QRS complex (ie, a terminal wide S wave is seen at the end of the QRS of each odd-numbered beat = beats #1,3,5 and 7).
• PEARL #5: The fact that the QRS of each of the even-numbered beats is narrow — suggests that the longer preceding R-R interval before beats #2,4,6,8 allowed enough additional time for recovery of right bundle branch conduction (ie, that the reason for intermittent QRS widening is the result of some form of rate-related RBBB block).

Figure-2: I've added BLUE arrows to highlight that every-other beat is wide (as per the wide terminal S wave in beats #1,3,5,7).

P waves are present!

I've highlighted with RED arrows in Figure-3 that an underlying regular atrial rhythm is present.

• You may or may not have initially seen P waves in all of the places where I've added RED arrows — because some of the P waves are partially hidden within the end of the QRS or within peaked T waves.
• PEARL #6: Use of calipers allows us to very quickly verify where all of the P waves lie. For example — we definitely see P waves under the 3rd and 4th RED arrows — and if we set our calipers to the P-P interval between these 3rd and 4th red arrows, we can "walk out" where the partially hidden P waves lie throughout the rest of the tracing.
• PEARL #7: I find the simple steps of numbering the beats and labeling the P waves (with arrows) — tremendously facilitates the next step in our assessment of the rhythm, which is to determine if P waves are Related to neighboring QRS complexes?
• NOTE (Beyond-the-Core): If you carefully measured all P-P intervals in Figure-3 — You may have noted slight variation in the atrial rate. Technically, this is the result of a slight ventriculophasic sinus arrhythmia — which is a common phenomenon in 2nd- and 3rd-degree AV blocks. That said, for practical purposes — We can say that the underlying atrial rhythm is essentially regular.

Figure-3: I've added RED arrows to highlight the regular atrial rhythm.

Are P Waves Related to Neighboring QRS Complexes?

The KEY step for determining if some form of AV block is present — is to determine if at least some P waves are Related to neighboring QRS complex?

• To do this — I survey the entire rhythm strip, looking to see if any PR intervals repeat? Once again — calipers greatly facilitate (and expedite) this step, since calipers enable us to very quickly tell if PR intervals are or are not varying in duration.
• In Figure-4 — I've added PINK arrows to highlight identical (albeit prolonged) PR intervals that are seen in front of beats #1,3,5,7.
• PEARL #8: The fact that at least some of the PR intervals in today's tracing repeat tells us that at least some beats are being conducted to the ventricles!

Figure-4: Pink arrows highlight P waves with identical (albeit prolonged) PR intervals that repetitively occur throughout the long lead II rhythm strip (ie, before beats #1,3,5,7).

Are Any More P Waves Conducting?

At this point — we know from Figure-4 that beats #1,3,5,7 are all being conducted with a long PR interval.

• As we continue to look at the PR intervals preceding the remaining beats — it should be apparent that the shorter PR intervals highlighted by RED arrows in Figure-5 are also all identical (ie, all equal to 0.16 second). 
• This tells us that each of these RED arrow P waves are also conducting to the ventricles.

Figure-5: RED arrows highlight P waves identical PR intervals

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Part 2: Putting It All Together ...

I've synthesized in Figure-6 what we've worked out thus far regarding today's ECG.

• Today's rhythm manifests an overall slow ventricular rhythm that is not regular. Instead — there is group beating in the form of a regularly irregular rhythm with alternating shorter-then-longer R-R intervals.
• There is an underlying regular atrial rhythm ( = the colored arrows in Figure-6).
• Many of the P waves in Figure-6 are conducting — albeit with 2 different PR intervals (highlighted by RED and PINK arrow P waves).
• But there clearly are more P waves than QRS complexes — with the result that lots of P waves are not conducting (ie, the YELLOW arrow P waves in Figure-6 are not conducting).
• In addition, there are 4 places in the long lead rhythm strip where consecutive P waves are not conducting (ie, neither of the consecutive YELLOW arrow P waves that are seen between beats #1-2; 3-4; 5-6; and 7-8 are conducting).

Impression:

• Some form of AV block is present — because we have a regular atrial rhythm, but not all of the on-time P waves are being conducted.
• We can immediately recognize that the rhythm is not complete AV block because: i) The ventricular rhythm is clearly not regular (whereas with complete AV block — there is usually a regular [or at least, almost regular] ventricular escape rhythm); — and, ii) The fact that the RED and PINK arrow P waves are conducting means that "complete" AV block can not be present because there is some conduction.
• Since AV block is not "complete" — the rhythm must represent some form of 2nd-degree AV block. And since there are consecutive on-time P waves that fail to conduct — today's rhythm represents a high-grade form of 2nd-degree AV block.

PEARL #9: Despite the length of my discussion up to this point — the clinically important conclusion (ie, that today's rhythm represents some form of high-grade 2nd-degree AV block with resultant bradycardia) — can be reached quickly, simply by noting the following:

• The ventricular rhythm is slow and irregular in the form of group beating.
• Regular P waves are present.
• Some PR intervals repeat — which means that at least some P waves are conducted. But many "on time" P waves fail to conduct, including several instances of consecutive "on time" P waves that fail to conduct.
• Therefore — some form of high-grade 2nd-degree AV block is present. Especially in view of the bradycardia — pacing may be needed if the rhythm persists. In the meantime — We need to find out the history. In addition — We need to carefully review the rest of the ECG to see if recent or ongoing ischemia/infarction is a likely cause of this AV block?

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What Type of 2nd-Degree AV Block is Present?

I've reviewed the 2nd-degree AV blocks in many posts on this ECG Blog (See ECG Blog #62 and ECG Blog #465 — with Video Review of these concepts in the Addendum of Blog #465). In brief — the 2nd-degree AV blocks are divided into the Mobitz I and Mobitz II forms. Reasons why today's AV block is almost certain to represent some form of Mobitz I ( = AV Wenckebach) include the following:

• i) Mobitz I is much more common than Mobitz II; 
• ii) As was seen in Figure-2 — the QRS complex of conducting beats is intermittently narrow — whereas the QRS is almost always consistently wide with the more severe Mobitz II form of 2nd-degree AV block; 
• iii) There is group beating, and as noted earlier in PEARL #3 — the presence of group beating in association with a regular atrial rhythm in which some beats are conducted but others are not — is often the result of AV Wenckebach ( = Mobitz I).
• iv) Mobitz I is very commonly associated with inferior and/or posterior MI — so another point in support of Mobitz I would be IF the 12-lead ECG was suggestive of recent or ongoing inferior and/or posterior MI. (In contrast — Mobitz II is more often associated with anterior MI).

Take another LOOK at today's 12-lead ECG in Figure-6.

• Is there evidence of recent or ongoing infarction?

Figure-6: Today's ECG. Is there evidence of recent or ongoing infarction?

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Is there Evidence of Recent Infarction?

As we established earlier — both the PINK and RED arrow P waves in the long lead II rhythm strip of Figure-6 are being conducted to the ventricles, albeit with different PR intervals.

• This means that beat #5 in lead V1 of Figure-6 is being conducted to the ventricles with RBBB (Right Bundle Branch Block) — whereas the longer preceding R-R interval before beat #6 allows enough extra time for recovery of normal conduction.
• Although some ST-T wave depression will normally be seen in anterior leads when there is RBBB conduction — the amount of ST-T wave depression in lead V2 (if not also in leads V1 and V3) appears to be disproportionately increased. This suggests recent posterior OMI as a likely cause of the Mobitz I conduction disturbance.

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My Proposed Laddergram for Today's Rhythm:

As I alluded to in my introduction to today's case — today's rhythm was complex enough such that I needed to draw a laddergram in order to precisely determine the etiology of this conduction disturbance.

• To emphasize (as stated in PEARL #9) — a laddergram is not needed to quickly derive the clinically important conclusion that bradycardia with high-grade Mobitz I 2nd-degree AV block is present, most probably as a result of recent posterior MI.
• That said — I find laddergram illustration of complex arrhythmia mechanisms insightful and helpful in understanding the physiologic process.
• For readers with an interest in learning how to draw laddergrams — I review my approach with over 100 illustrated cases in ECG Blog #188.
• To emphasize that although it takes time and practice to become comfortable drawing laddergrams — with minimal instruction, it becomes EASY to understand even complex laddergrams that are already drawn for you. This should become evident with explanation of my proposed laddergram for today's case.

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Therefore — I conclude today's case with laddergram derivation of the group beating pattern that we recognize in today's tracing.

Figure-7: Laddergram STEP-1. It is usually easiest to begin a laddergram by filling in the Atrial Tier. Here — GREEN arrows show the onset of P waves as my reference point for drawing in atrial activity. Because conduction through the atria is generally rapid — I draw near-vertical lines in the Atrial Tier to represent this.

Figure-8: Laddergram STEP-2. I next fill in the Ventricular Tier. BLUE arrows show the onset of each QRS complex as my reference point for each of the QRS complexes in this tracing.
= = = = = = =
KEY Point: The "EASY part" for constructing most laddergrams consists of these first 2 STEPS (that are shown in Figures-7 and -8). Now the challenge begins — for trying to "solve" the laddergram by figuring out which of the P waves in the Atrial Tier are being conducted to the ventricles.

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NOTE (Beyond-the-Core): Because consecutive non-conducted P waves are seen in several places in today's tracing — I suspected that there may be dual-level AV block within the AV Node (I explain and illustrate this advanced concept in ECG Blog #463). It is for this reason that I divide the AV Nodal Tier into 2 parts (by drawing in a horizontal BLACK dotted line in Figure-9).

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Figure-9: Laddergram STEP-3. Whle realizing that many complex tracings may have more than a single potential laddergram explanation — I begin my derivation of conduction through the AV Nodal Tier by drawing in the path of those P waves that I know are conducting. In today's case — this will consist of the RED and PINK arrow P waves.

Figure-10: As was shown in Figure-5 — the constant normal PR interval (of ~0.16 second) suggests that RED arrow P waves in today's tracing are normally conducted to the ventricles. As a result — these RED arrow P waves are the first P waves that I connect to neighboring QRS complexes within the Ventricular Tier (ie, to beats #2,4,6,8).

Figure-11: As was shown in Figure-4 — the constant but much longer PR interval of PINK arrow P waves suggests that beats #1,3,5,7 are also conducted to the ventricles — but much more slowly than conduction of the RED arrow P waves. I illustrate this by an increase in angulation as these impulses pass through both parts in the AV Nodal Tier (BLUE lines). As is often the case — conduction of impulses through the dual parts of the AV Nodal Tier is slower through the lower part.

Figure-12: As we look at the laddergram in Figure-11 — We see that each of the 8 conducted beats in today's tracing has already been assigned to a P wave that conducts to the ventricles. This tells us that none of the remaining P waves (ie, none of the YELLOW arrow P waves in Figure-12) make it through the AV Nodal Tier to the ventricles. Therefore — the remaining STEP in developing my proposed laddergram is to postulate a logical mechanism by which conduction might be halted within the AV Nodal Tier.
= = = = = = =
It seems logical to postulate that the single YELLOW arrow P waves that occur within the shorter R-R intervals (ie, between beats #2-3; 4-5; 6-7) do not make it through the upper AV Nodal level (BLUE butt-ends that I've drawn in this upper AV Nodal level).

 

Figure-13: As we look at the laddergram in Figure-12 — We see that a repetitive pattern remains for the 2 unattached YELLOW arrow P waves within each of the longer R-R intervals. So — If I can figure out a logical mechanism by which conduction might be halted within one of these longer R-R intervals — the same mechanism will probably apply to the 3 other longer R-R intervals.
= = = = = = =
NOTE: Sometimes I simply need to "try out" several possibilities by "trial and error" — until I find one that works. I illustrate this process in Figure-13 — in which I postulate 3:2 AV conduction through the upper AV Nodal level — and then 2:1 AV conduction through the lower AV Nodal level (BLUE lines within the AV Nodal Tier).

Figure-14: Since the BLUE lines that I drew within the AV Nodal Tier in Figure-13 appear to be the most logical solution for the path of conduction for the 2 YELLOW arrow P waves within beats #1-2 — I repeat this sequence as the likely conduction path occurring within the remaining 3 longer R-R intervals.

Figure-15: My completed laddergram. Today's rhythm is most consistent with high-grade 2nd-degree AV block, with dual-level Wenckebach conduction out of the AV Node. 

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Final Thoughts:

As I speculate in my explanation of Figure-6 — I suspect recent posterior OMI as the cause of today's conduction disturbance.

• Alternatively — it's possible that the disproportionately increased anterior lead T wave inversion in Figure-6 might represent an LAD "culprit" in a patient with multi-vessel disease, now with some evidence of spontaneous reperfusion. 
• In either case, prompt cath to define the anatomy, with PCI reperfusion if a "culprit" artery is identified — would seem the preferred management approach. 
• The "good news" is that if PCI is successful in reperfusing a "culprit" artery — then the high-grade AV block with resultant bradycardia (as well as the intermittent rate-related RBBB) might both resolve. 

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Acknowledgment: My appreciation to Omar Hassan Seddik (from Mansoura City, Egypt) for submission of today's case with these tracings.

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ADDENDUM (6/20/2026):

Those of you who frequent various international ECG forums will probably be familiar with periodic commentary from David Richley, whose expertise in complex arrhythmia interpretation is renowned. So I always welcome Dave's insights on complex cases that I post. He has just sent me the following comment with a proposed alternative to my laddergram in Figure-15.

Dave wrote the following:

• Hi Ken. I love the superb ECG you just posted in your blog and agree with your dual-level AV nodal Wenckebach block explanation. Your laddergram seems to show 3:2 alternating with 2:1 block at the upper AV node, with 3:2 block at the lower AV node. 
• I couldn’t see why the conduction ratios should alternate in this manner at the upper AV node, so I thought I’d see if I could come up with something a bit simpler. My slightly different explanation is that there is 5:4 block at the upper node — and 2:1 block at the lower node (See Figure-16 below for Dave's alternative laddergram). 
• I realize that this is purely speculative and cannot be proved — and that there may well be other theoretically possible conduction patterns to explain the ECG. Also, of course, it is of no clinical importance — but I thought you might be interested in this slight variation on your excellent interpretation — Dave.

 

Figure-15: David Richley's proposed laddergram for today's case.

My Thoughts on David Richley's Comment:

• I especially like Dave's comment — because it supports a point that I often make, namely that more than a single plausible explanation is possible for many complex arrhythmias. Dave's proposed alternative laddergram in Figure-16 is certainly plausible.
• I still favor my own laddergram — as I don't see 5:4 conduction in the upper AV nodal level as being "a simpler explanation". That said — it may well be that Dave's laddergram is correct and mine isn't (or vice versa).
• Practically Speaking (as Dave acknowledges) — We can not prove which laddergram is the more precise one.
• Clinically — We both agree there is high-grade 2nd-degree AV block of the Mobitz I Type, which is the key information needed for appropriate clinical management.
• Academically — I find discussion of arrhythmia mechanisms fascinating and insightful — as delving into these details fine tunes my abilities in arrhythmia interpretation.
• That said

ECG Blog #533 — A Wide Tachycardia

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Please NOTE: 

• I am back! My weekly ECG Blog posts resume this week (and I'll eventually catch up with ECG correspondence sent to me while I was gone).
• Below — a 40-second video clip that I made of Niagara Falls, up close from the Canadian side ( = 1 of the many sites I was privileged to see).

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THANK YOU all for your interest & continued support!

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ECG Blog #533 — A Wide Tachycardia ... 

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The ECG in Figure-1 was obtained from a previously healthy 60-something year old man — who sought medical care for the abrupt onset of “palpitations”. The patient was hemdynamically stable at the time this ECG was recorded.

QUESTIONS:

• How would YOU interpret the ECG in Figure-1?
• What would you do? 

Figure-1: The initial ECG in today's case — obtained from 60-something year old patient. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts:

The “good news” — is that the patient is hemodynamically stable at the time this ECG was recorded. As a result — We have at least a moment in time to assess the tracing before we would need to begin treatment. 

• As always, I like to start with assessment of the rhythm — for which I favor the P’s,Q’s,3R Approach for optimal time-efficient rhythm interpretation (See ECG Blog #185 — for review of the Ps,Qs,3R Approach).
• The ECG in Figure-1 lacks a long lead rhythm strip. That said, we can still interpret the rhythm — beginning with whichever of the 5 KEY parameters is easiest to assess.
• The rhythm in today’s ECG is Regular. 
• The Rate is fast, at about 170/minute.
• The QRS is wide (ie, clearly more than half a large box in duration — and probably ~0.12 second in duration).
• With regard to P waves — there is no clearly upright P wave deflection in lead II — and in general, the fast rate and large ST-T waves seem capable of “hiding” atrial activity within them. 

My Impression from the Ps,Qs,3Rs: 

In this 60-something year old man with palpitations (about whom we do not yet know anything regarding his medical history) — The rhythm in Figure-1 is a regular WCT (Wide-Complex Tachycardia) at ~170/minute, but without clear sign of sinus P waves.

The differential diagnosis includes the following:  

• i) VT (Ventricular Tachycardia) — which always needs to be assumed for any regular WCT rhythm without sinus P waves until proven otherwise.
• ii) Sinus Tachycardia (with sinus P waves being hidden within the giant T waves that precede each QRS complex).
• iii) An SVT (SupraVentricular Tachycardia) reentry rhythm (ie, most commonly AVNRT or AVRT). 
• iv) AFlutter (Atrial Flutter).
• v) ATach (Atrial Tachycardia).

PEARL #1: To emphasize that although I've described my above assessment in “slow motion” — With practice, all that I’ve written above should be noted and considered within less than 1 minute!

• Because this patient is hemodynamically stable — We can take a few extra moments to see what additional clues might be present to help us narrow down our differential diagnosis.
• Statistically — in an unselected adult population of a "certain age" — at least 80% of regular WCT rhythms without clear sign of sinus P waves will turn out to be VT. 
• That said — 80% is not 100%. Therefore, if your patient is hemodynamically stable — this means that we still have a moment to look for additional clues to the etiology of the rhythm. Two of my “favorite potential clues” to look for are: 
• i) Is there any sign of atrial activity? — and, 
• ii) QRS morphology.

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Is there any sign of Atrial Activity?

Take another LOOK at the ECG in Figure-1.

• Keep in mind that sinus P waves should be upright in lead II — whereas retrograde P waves are almost always negative in one or more of the inferior leads.
• 
  
• What do YOU see? 

ANSWER:

It turns out that there is atrial activity in today's ECG — in the form of 1:1 V-A (retrograde) conduction (YELLOW arrows in Figure-2).

• Although this retrograde atrial activity is only seen in one of the inferior leads — it's hard to imagine what else this slender spike that occurs toward the end of the QRS in lead II could be other than a retrograde P wave.
• As suggested by the parallel RED timeline — these retrograde P waves clearly fall within the QRS complex, which explains why retrograde P waves might not be seen in other leads.
• P.S.: We now have an answer to the 5th parameter of the Ps,Qs,3Rs — which is the 3rd "R" = Related. So there is atrial activity, in the form of retrograde P waves that manifest a constant relationship ( = Related by a fixed RP' interval) to neighboring QRS complexes = 1:1 retrograde conduction.

PEARL #2: It's important to appreciate that the finding of 1:1 VA conduction does not distinguish between VT vs an SVT rhythm. This is because both reentry SVTs and VT may manifest 1:1 retrograde conduction.

• But IF today's rhythm is supraventricular — then it is almost certain to represent AVNRT (AV Nodal Reentrant Tachycardia) because:
• These P waves are not upright in lead II — so assuming no lead reversal, the rhythm cannot be sinus tachycardia.
• There is no sign of 2:1 AV conduction — so this is not AFlutter.
• It seems unlikely that ATach would manifest a negative P wave in only lead II with such a long RP interval.
• The other form of reentry SVT, which is AVRT ( = AtrioVentricular Reciprocating Tachycardia) generally has a longer RP' interval — with the retrograde P wave occurring later in the ST segment because of the greater amount of time needed to complete a reentry circuit that includes an AP (Accessory Pathway) that lies outside the AV Node (as I illustrate and discuss in ECG Blog #240).

Figure-2: I've labeled the retrograde P waves in today's ECG.

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Does QRS Morphology provide any Clue?

Practically speaking — aberrant conduction is most likely to take the form of some type of bundle branch block and/or hemiblock pattern. As discussed in ECG Blog #211 — although RBBB (Right Bundle Branch Block) aberration is the most common form — you can also see rate-related aberrant conduction that manifests LBBB and/or either pattern of hemiblock conduction (LAHB or LPHB — with or without RBBB).

• As emphasized in ECG Blog #204 — the 3 KEY leads for the ECG diagnosis of the bundle branch blocks are right-sided lead V1 — and left-sided leads I and V6.
• Assessment of these 3 KEY leads during the WCT rhythm in today's case is consistent with LBBB morphology — because we do see an all upright QRS in lateral leads I and V6 — and the QRS is predominantly negative in right-sided lead V1, with a steep S wave downslope in the anterior leads (as discussed in ECG Blog #346).

PEARL #3: While I was in no way certain of the diagnosis — as soon as I appreciated that QRS morphology in Figure-2 is perfectly consistent with LBBB conduction — I suspected that this regular WCT rhythm was probably supraventricular!

• KEY Point: We often need to begin treatment of the patient in front of us before we are 100% certain of the etiology of the rhythm. So although we still could not rule out the possibility of VT on the basis of this single ECG — since the patient was hemodynamically stable, using Adenosine as a diagnostic-therapeutic trial would seem an excellent option (ie, Adenosine should convert the rhythm if it is AVNRT or AVRT — and it may facilitate diagnosis of AFlutter or ATach by momentarily slowing the rate) — being ready to cardiovert if at any time the patient were to become unstable.
• 
  
• PEARL #4: The most common form of VT that manifests a QRS morphology resembling LBBB conduction in the chest leads — is RVOT VT (Right Ventricular Outflow Track VT). That said — strongly against RVOT VT in today's case is the lack of an inferior frontal plane axis (See ECG Blog #525 — for review of RVOT VT).

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CASE Follow-Up:

I subsequently learned of this patient's history:

• There was no history of coronary disease.
• Instead — the patient had a long history of arrhythmias, having undergone an ablation for a resistant SVT rhythm a number of years earlier.
• He was now being admitted to the hospital for a recurrence of his symptoms — and was scheduled for elective ablation the next day — when he developed the rhythm in Figure-1. This tachycardia easily converted to sinus rhythm following an initial 6 mg IV dose of Adenosine.
• EP study then revealed a concealed AP (Accessory Pathway) — but no inducible tachycardia. Instead — a "fast-slow" AVNRT was induced and ablated (this AVNRT rhythm being consistent with the short RP' interval highlighted by the YELLOW arrows in Figure-2).
• The LBBB morphology seen in Figure-2 was found to be the result of rate-related LBBB aberrant conduction. Conduction with a normal QRS complex resumed once the heart rate slowed following ablation.

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Acknowledgment: My appreciation to @PrecordialSwirl for submission of today's case with these tracings.

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ECG Blog #532 — A Surprise Diagnosis ...

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Please NOTE: 

• After today — No new ECG Blog posts for ~4 weeks ...
•     — I will also not be prompt in replying to emails ... 

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All material on this ECG Blog site remains open!

• The INDEX tab (in the upper right of each page) — has linked Contents, listed by subject. So IF you are looking for ECG material — There is plenty on this web site!
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THANK YOU all for your interest & support!
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ECG Blog #532 — A Surprise Diagnosis ... 

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The ECG in Figure-1 was obtained from a middle-aged man — who presented to the ED (Emergency Department) with a 1-week history of intermittent "burning chest pain" — with some "shortness of breath".

QUESTIONS:

• How would YOU interpret the ECG in Figure-1?
• Should you activate the cath lab?
•   — Should you do anything else at the bedside?

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

MY Thoughts:

The ECG in Figure-1 was sent to me with the above history. I wrote back that my initial interpretation of this tracing was the following:

• This is a very worrisome ECG!
• There is sinus tachycardia — which of itself is a worrisome sign, since sinus tach tends to be an uncommon finding with acute MI — unless "something else" is going on (ie, heart failure, shock, etc.).
• There are inferior Q waves in a "qRS" pattern — which in the inferior leads usually means that an inferior MI has occurred at some point in time.
• At the least — there is DSI (Diffuse Subendocardial Ischemia) — as indicated by ST elevation in lead aVR, with ST depression in the other 5 limb leads (as well as in the lateral chest leads).
• I suspect there is a Precordial "Swirl" pattern — with clearly abnormal ST elevation and T wave inversion in lead V1 — and ST segment straightening with ST elevation in leads V2,V3 — and what looks to be some J-point depression in lead V6 (A "Swirl" pattern is typically seen with acute or recent proximal LAD occlusion — and the loss of R wave from V2-to-V3 suggests anterior infarction).

The difficult question is what is "new" vs "old" — and, if "new" (as I suspect) — How "new" given the 1 week history of intermittent CP?

• I asked the following: i) Any prior history of heart disease in this patient? — and, ii) Any prior ECGs available?
• I suggested that, "The patient needs prompt cath" — with my suspicion of an LAD "culprit" artery.

QUESTION:

• BUT — What did I not mention in my above comments? 

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CASE Follow-Up:

• The patient was admitted to the Intensive Care Unit with a diagnosis of acute ACS (Acute Coronary Syndrome).
• While contemplating the best approach to management — bedside Echo was done. Surprisingly — bedside Echo showed a markedly dilated RV with a "D-shaped" septum.
• CTPA (CT Scan Pulmonary Angioram) was then performed — which confirmed the diagnosis of massive acute PE (Pulmnary Embolism).
• The patient was treated with injection of low molecular weight heparin (Enoxaparin) — and rapidly improved.

PEARL #1: Bedside Echo is a non-invasive, amazingly helpful diagnostic tool in emergency medicine — that with training, can be performed within minutes (and without which — the correct diagnosis in this otherwise puzzling case would have been delayed for hours!).

• Bedside Echo can be extremely helpful in confirming acute MI when ECGs are equivocal — IF — Echo shows a localized wall motion defect.
• The caveat is that if the patient is no longer having CP (Chest Pain) at the time that Echo is done — then nothing is ruled out if the Echo is normal. But if CP persists and the Echo shows perfectly normal LV function — this makes an acute MI much less likely.
• Bedside Echo may suggest Takotsubo Cardiomyopathy if there is "apical ballooning" due to apical akinesis or hypokinesis with preserved or hypercontractile basal segments (Izumo and Akashi — Cardiovasc Diagn Ther 8(1):90-100, 2018).

BOTTOM Line: Bedside Echo can provide invaluable assistance for strongly suggesting acute PE as the cause of your patient's symptoms — and it does so in a matter of minutes! 

• In today's case — Echo was the KEY Clue that led providers away from the diagnosis of ACS (Acute Coronary Syndrome) — and to the correct clue of massive acute PE! (See ECG Blog #443 — for a case in which I review the findings of Bedside Echo and CTPA in a patient with a large acute PE). 

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What Did We Miss?

In cases like this one — I find it helpful to "soul-search" and GO BACK to try and learn from any clinical clues that may have been missed.

• "Some shortness of breath" was mentioned in the brief history we were given. It's hard to know how significant the symptom of dyspnea was in today's case from words on the printed page. Sometimes — "Ya just gotta be there!" ( = at the bedside!).
• PEARL #2: In my experience — by far, the most commonly overlooked vital sign is the respiratory rate! Much of the time — the clinician at the bedside simply does not take the time to COUNT the respiratory rate. 
• Nurses also (in my experience) do not always count the respiratory rate. Instead — they sometimes just put down 12 or 15/minute if the patient "seems OK".
• Clinical Reality: Unless you spend a conscious moment in which you truly LOOK at the patient — it is all-too-easy to miss a patient taking small but rapid breaths — unless you actually COUNT the breaths per minute. And if the patient was breathing 25-30/minute at rest ==> that's tachypnea, which should serve as an important clue that an acute pulmonary problem may be the cause!

Taking Another Look at Today's ECG ...

In addition to the history of CP (described as a "burning" chest pain in today's case) — the ST elevation in the anterior leads in the initial ECG (in Figure-1) led me to suspect an acute cardiac event as my primary diagnosis.

• PEARL #3: Instead of the anterior ST depression or T wave inversion of RV "strain" — anterior lead ST elevation may sometimes be seen with acute PE (Zhan et al — Ann Noninvasive Electrocardiol 19(6):543-551, 2014 — and — Omar HR — Eur Heart J: Acute Cardiovascu Care (5(8): 579-586, 2016). 
• Right-sided leads such as leads III, aVR and V1 — face the anterior region of the RV. If the RV is enlarged — then leads V2 and V3 may also face the anterior region of the RV — and — if there is severe transmural ichemia of the RV, any of these leads may show ST elevation (as is seen in leads aVR and V1,V2,V3 in today's initial ECG).

What I also found confusing about the initial ECG in today's case — was the question of whether there is (or is not) ST depression in multiple leads.

• The answer to this question depends on how you define the ST segment baseline — which sometimes is not an easy task.
• As review — I include below in Figure-2 my approach for determining the ST segment baseline in any given tracing.

   

Figure-2: "My Take" on defining the ST segment baseline (from Grauer K: ECG Pocket Brain-2014 ePub).

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With PEARL #3 and Figure-2 in mind — I'll add Figure-3 below, which is my summarizing chart of the ECG Findings associated with acute PE — which I then reapply to today's initial ECG in Figure-4.

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Figure-3: ECG Findings associated with acute PE (updated since ECG Blog #443).

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Figure-4: Another Look at Today's Initial ECG ...

 

Figure-4: I've labeled today's initial ECG.

KEY Point: With the above information in mind — Today's ECG (that I've labeled in Figure-4) — could be consistent with the diagnosis of acute PE, albeit without the typical appearance of RV "strain", in which T wave inversion is seen in anterior and/or inferior leads. Among the ECG findings in Figure-4 potentially consistent with acute PE are the following:

• Sinus tachycardia (Here at a rate of ~115/minute).
• S waves in multiple leads (ie, Leads I,II,III; aVF; V4,5,6).
• ST elevation in lead aVR.
• RV "strain" (Here in the form of ST depression in the inferior leads — assuming one uses the TP baseline for judging if there is ST elevation or depression).
• Anterior lead ST elevation — which as noted in PEARL #3, can be a sign of acute PE.
• ST depression in the remaining chest leads (V4,V5,V6) — again assuming one uses the TP baseline for judging if there is ST depression.

PEARL #4: ECG findings in Figure-4 against acute PE are: i) Q waves in each of the inferior leads (YELLOW arrows in leads II,III,aVF); — and, ii) Loss of r wave between lead V2-to-V3, with a QS wave in lead V3.

• In this patient who presented with a 1-week history of "burning" CP and some "shortness of breath" — this ECG leaves us with trying to distinguish between acute LAD occlusion vs acute PE (with the additional possibility of Takotsubo Cardiomyopathy — given diffuse ST-T wave abnormalities, and what appears to be a prolonged QT interval).
• KEY Point: Until bedside Echo was done in today's case — I strongly suspected acute proximal LAD occlusion as the diagnosis.

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"Take Home" Message:

On occasion — acute PE may present with a "pseudo-infarction pattern, as it did in today's case.

• Bedside Echo made the diagnosis in a matter of minutes.

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Acknowledgment: My appreciation to Mohammed Elsisi (from Cairo, Egypt) for the case and these tracings.

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #443 and ECG Blog #496 — Review challenging cases on the ECG diagnosis of acute PE.
• ECG Blog #313 and ECG Blog #435 — Review more cases on the ECG diagnosis of acute PE.
• ECG Blog #233 — Reviews a case of Acute PE (with discussion of ECG criteria for this diagnosis).
• ECG Blog #119 — Reviews a case of Acute PE (and ECG criteria for this diagnosis).
• My Comment at the bottom of the page in the June 17, 2024 post in Dr. Smith's ECG Blog (regarding a case similar to today's ECG Blog).
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• ECG Blog #234 — Reviews ECG criteria for the diagnosis of RVH and RV "Strain".
• ECG Blog #77 — Another review of ECG criteria for the diagnosis of RVH and RV “Strain”. 
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• ECG Blog #380 — Reviews the concept of Precordial "Swirl".
• ECG Blog #483 — Reviews the concept of DSI (Diffuse Subendocardial Ischemia) in Pearl #1 of this blog post.