Friday, October 11, 2024

ECG Blog #451 — Premature Closure ...


I was sent the ECG shown in Figure-1 — told only that the patient was a middle-aged man with septicemia.


QUESTIONS: 
  • Is this rhythm too fast to be sinus tachycardia?
  • Are flutter waves hidden within the QRS and T waves?
  • Are we seeing the retrograde P waves of AVNRT?
  • Is this ATach (Atrial Tachycardia)?

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

MY Thoughts on Today’s CASE:
In my opinion — none of the above answers are optimal to describe the rhythm in Figure-1. I say this for the simple reason that to pick any of the above 4 choices — is to imply with 100% certainty that you know the answer (or, as is implied in the title of today’s Blog post — this would be premature closure).
  • Instead, I feel it preferable to openly acknowledge that — We do not know for certain what the rhythm is

The above said — I did have a good idea what this rhythm was most likely to be. However, until such time that we know for certain — I think it best to simply describe what we see:
  • PEARL #1: Realize that for any tachycardia — there are 6 Parameters that need to be assessed. The 1st Parameter — is to ensure that the patient is hemodynamically stable. This is because IF your patient is not stable — then it no longer matters what the rhythm is (because immediate cardioversion will be needed — regardless of whether the rhythm is VT or an SVT).
  • Next (assuming your patient is hemodynamically stable) — Assess the rhythm for the remaining 5 KEY Parameters — that are most easily remembered by the saying, “Watch your Ps, Qs — and the 3Rs”. With practice — it should literally take no more than seconds to assess these 5 Parameters (See ECG Blog #185 — for more on the Ps,Qs,3R Approach to rhythm interpretation).


Watch your Ps, Qs — and the 3Rs:
Regarding today's initial rhythm — I see the following:
  • There is significant artifact, especially in leads V1,V2 (See Figure-2). This makes assessment of P waves impossible in these 2 chest leads. 
  • That said — I thought sinus P waves might be present in the inferior leads. However, I could not with certainty distinguish between what might be a P wave? — vs a T wave? — vs a P wave hiding within the preceding T wave (ie, under the ?'s that I placed in the inferior leads).
  • On the other hand — Doesn't it look like there might be 2:1 atrial activity in lateral leads V5,V6 (slanted RED lines in these leads)? As a result — I was not certain about the presence and/or nature of atrial activity.
  • NOTE: My "Go-To" Leads when looking for extra atrial activity are leads II,III,aVF; aVR; and V1 — which is why I was not convinced on the basis of the RED lines I drew in Figure-2 that this truly represented 2:1 atrial activity.

Continuing with the 5 Parameters:
  • The rhythm in Figure-2 is Regular — at a Rate of ~160/minute (ie, with an R-R interval slightly less than 2 large boxes in duration).
  • The QRS complex is narrow in all 12 leads (ie, Not more than half a large box in any of the 12 leads).
  • The last of the 5 Parameters — is whether P waves are Related to the QRS complex. But since we are not certain if there even is atrial activity? (and if so — whether such atrial activity represents sinus P waves, flutter waves, or something else?) — we can not yet address this 5th Parameter.

  • BOTTOM Line: Today's initial rhythm is a regular SVT (SupraVentricular Tachycardia) at ~160/minute, but without clear indication of the presence and nature of atrial activity.

PEARL #2: Recognition that the rhythm in Figure-1 is a regular SVT — but with uncertainty regarding atrial activity — should prompt consideration of the followling differential diagnosis LIST (See ECG Blog #240):

  • i) Sinus Tachycardia (if sinus P waves are hidden below the ?'s in Figure-2 ). 
  • ii) A reentry SVT (either AVNRT if the reentry circuit is contained within the AV node — or AVRT if an accessory pathway outside the AV node is involved)
  • iii) Atrial Tachycardia (ATach);
  • iv) Atrial Flutter (AFlutter) with 2:1 AV conduction.
KEY Point: Although other entities may also produce a regular SVT (ie, sinoatrial node reentry tachycardia, junctional tachycardia) — they are far less common in practice. Therefore, remembering to think of the 4 entities in the above LIST whenever you encounter a regular SVT rhythm without clear indication of atrial activity — will greatly facilitate determining the correct diagnosis.


PEARL #3: Consider the History:
  • Is the patient on any antiarrhythmic medication? (This is important to consider — as it may affect the rate and conduction properties of the SVT).
  • Any known history of similar rhythms?
  • What is the clinical situation? (ie, In today's case the patient has septicemia — therefore seemingly susceptible to sinus tachycardia!).


PEARL #4: Consider the Rate of the SVT:

  • In adults — Sinus Tachycardia usually does not exceed 160-170/minute in a "horizontal" patient (ie, in a patient you are examining, who has not just been running). This is not to say that sinus tachycardia will never go faster than 170/minute — but rather to suggest that when the rate of the regular SVT rhythm you are assessing is well over this rate range — then the rhythm is less likely to be sinus tachycardia. NOTE: All bets are off in children — in whom sinus tachycardia over 200/minute is not that uncommon.
  • With AFlutter — the most common ventricular response in the patient who is not being treated with an antiarrhythmic medication is ~150/minute (usual range ~140-160/minute). This is because the atrial rate in untreated AFlutter is most often ~300/minute (usual range ~250-350/minute) — and since untreated AFlutter most often presents with 2:1 AV conduction — 300/2 ~150/minute. As a result — IF the ventricular rate of the regular SVT rhythm you are assessing is over ~170-180/minute (but under ~250/minute) — then AFlutter is less likely (because this rate would be faster-than-expected for 2:1 AV conduction, and too slow for 1:1 AV conduction)
  • NOTE: This ~140-160/min. range is for untreated AFlutter. Patients who are already on antiarrhythmic medication may present with a slower atrial rate (and therefore slower ventricular response) for AFlutter.
  • It is well to remember that ATach is less common as a cause for a strictly regular SVT, especially in an otherwise healthy young-to-middle-aged adult. ATach is more likely to be seen in patients referred for EP (ElectroPhysiologic testing) — and in older adults with SSS (Sick Sinus Syndrome). I include ATach in the above differential diagnosis LIST for completeness — but take into account that it won't be seen as often as AFlutter and the reentry SVTs.
  • Therefore — IF the rate of a regular SVT without clear sign of sinus P waves is substantially faster than 160-170/minute — then a reentry SVT rhythm (ie, AVNRT or AVRT) becomes the most likely diagnosis. 
  • But — IF the rate of the regular SVT is close to 150/minute (as it is with today's initial rhythm at ~160/minute) — then any of the 4 diagnostic entities in the above LIST could be present!


PEARL #5: Other potentially helpful considerations:  

  • Look for Atrial Activity! — which we've already addressed for today's rhythm (See above). Using calipers can facilitate your search for atrial activity.
  • Look for a “Break” (or subtle change) in the Rhythm! — Even a slight pause in the SVT rhythm, may be all that is needed to reveal underlying atrial activity that had been hidden by the regular tachycardia. There is no "break" in the rhythm in Figure-2. That said, it may be helpful to search Telemetry — as there may have been some change in the rhythm a little earlier in the patient's course.
  • Look for the “Onset” (and/or Termination) of the Rhythm! — The KEY clue to the etiology of an SVT often lies with capturing either the beginning and/or the end of the SVT. 
  • ATach often begins gradually, with progressive acceleration of the ectopic focus (ie, “warm-up” phenomenon). Then, there may be gradual slowing (ie, “cool-down) of the rhythm as it ends. 
  • In contrast — SVT reentry rhythms often start with 1 or more PACs that block conduction down one of the AV nodal pathways, which serves to set up the reentry circuit as the impulse starts down the other pathway. As a result — the onset of a reentry SVT is often abrupt (ie, accounting for the previous term used to designate this rhythm = PSVT = Paroxysmal SVT)The termination of reentry SVT rhythms is also usually quick (though this may occur over several beats).
  • Finally, when Sinus Tachycardia is suspected clinically (as it is in today's case) — awareness that over time the rate of sinus tachycardia will often change (become slower or faster) as the patient's condition becomes better or worse.

 
PEARL #6: While our goal is to arrive at as precise of a rhythm diagnosis as possible — the "good news" is that for practical purposes — initial diagnostic and/or treatment measures in the field or in the ED for an undifferentiated regular SVT rhythm are similar (ie, consideration of a vagal maneuver — and/or use of an AV nodal blocking agent such as Verapamil/Diltiazem; a ß-Blocker, and possibly Adenosine).
  • P.S.: If you suspect that the regular SVT rhythm is likely to be sinus tachycardia — then rather than antiarrhythmic medication, simply treating the underlying disorder may be all that is needed.

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


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Today's CASE Continues:
The patient was treated for sepsis. A very lose dose of IV Metoprolol was given. The repeat ECG is shown below in Figure-3.
  • What has happened?

Figure-3: The ECG was repeated after beginning treatment for sepsis.


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ANSWER — and CASE Conclusion: 
To facilitate comparison in Figure-4 — I've put together both ECGs in today's case.
  • Following treatment for sepsis — the patient improved clinically. As a result — the heart rate in ECG #2 has now slowed just enough to allow clear distinction of sinus P waves (RED arrows in lead II of the repeat ECG).
  • Clear distinction of sinus P waves is now also seen in each of my "Go-To" Leads (BLUE arrows in these leads), as well as in virtually all leads on this tracing.
  • Comparing ECG #2 with the initial tracing — We can see that sinus P waves were present the entire time! Because of the very fast rate in ECG #1 — the sinus P waves were simply hidden within the terminal part of preceding T waves.
  • Otherwise, on the repeat ECG — there are some nonspecific ST-T wave abnormalities (potentially rate-related) — and the possibility of large U waves (hard to tell — given the still rapid heart rate of 140-150/minute). Serum K+ and Mg++ levels need to be verified.

Figure-4: Comparison of the repeat ECG with the initial ECG (after treatment of sepsis).


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Acknowledgment: My appreciation to Sam Ghali @EM_RESUS (from Jacksonville, Florida — USA) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case: 

  • ECG Blog #185 — Reviews the Ps, Qs & 3Rs Approach to systematic rhythm interpretation.
  • ECG Blog #188 — Reviews the essentials for reading (and/or drawingLaddergrams, with LINKS to numerous Laddergrams I’ve drawn and discussed in detail in other blog posts.

  • ECG Blog #240 — The regular SVT ...
  • ECG Blog #229 — Why is AFlutter so commonly overlooked?
  • ECG Blog #138 — AFlutter vs Atrial Tachycardia
  • ECG Blog #40 — Another regular SVT that turned out to be AFlutter.

Other sites where I've discussed similar cases:

  • The March 6, 2020 post in Dr. Smith's ECG Blog.
  • The October 16, 2019 post in Dr. Smith's ECG Blog. 
  • Please check out the November 12, 2019 post in Dr. Smith's ECG Blog — in which I reviewed the case of a different kind of regular SVT Rhythm (AFlutter).


 







Friday, October 4, 2024

ECG Blog #450 — A "Healthy" 30yo with Dizziness


The ECG shown in Figure-1 was obtained from a previously healthy 30-year old man — who had this ECG as part of a "routine" pre-employment physical exam. He has had a few episodes of "dizziness", but no syncope. He is otherwise well without medical problems.


QUESTIONS:
  • How would YOU interpret the ECG in Figure-1?
  • How to evaluate this patient?

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:
This is a challenging tracing to interpret — because there is marked bradycardia with an irregular rhythm and a change in QRS morphology.
  • There are only 8 beats recorded on this ~10 second rhythm strip — for an average rate of ~50/minute.
  • The QRS complex is wide (ie, >0.10 second in duration).
  • A number of sinus P waves are present — as well as what appears to be some P waves arising from a different atrial site.

At this point — I thought it would be most helpful to identify atrial activity — which I have done with colored arrows in Figure-2.
  • Upright sinus P waves are seen before beats #1,2,3,4; and #7,8 in the long lead II rhythm strip (RED arrows) — with this rhythm strip having been simultaneously recorded with the 12-lead tracing above it. The PR interval in front of each of these 6 beats is constant at ~0.12 second — such that these are sinus-conducted beats (0.12 second being the lower limit of normal for conduction through the atria).
  • The widened qRS complex that follows each of these sinus-conducted beats in left-sided leads I and V5,V6 — suggests that these beats are conducted with RBBB (Right Bundle Branch Block).
  • Small amplitude negative deflections are seen to occur after the T waves of beats #4 and 5. These appear to be non-conducted P waves  since they are not followed by any QRS complex (PINK arrows in Figure-2). Since the shape of these negative deflections differs from the shape of the RED arrow sinus P waves — I though these PINK arrow P waves were arising from a different site in the atria.
  • There is no P wave in front of beat #5. Since the QRS morphology of this beat #5 in the long lead II, looks to be the same as the QRS morphology of sinus beats #1,2,3,4; and 7,8 — beat #5 must be a junctional escape beat.
  • Note that the rSr’ morphology of beat #5 in simultaneously-recorded lead V1 — supports my suspicion that sinus beats #1,2,3,4; 7,8 are conducted with RBBB.
  • This leaves us with beat #6 — that is also wide, not preceded by any P wave in the long lead II rhythm strip — and different in QRS morphology than the other 7 beats in the long lead II rhythm strip that manifest RBBB conduction. This suggests that beat #6 is a ventricular escape beat.

IMPRESSION: Today’s initial ECG is a complex tracing that manifests marked sinus bradycardia and arrhythmia — underlying RBBB — and both junctional and ventricular escape beats when the heart rate drops below 50/minute.
  • There also appears to be some non-conducted P waves arising from another atrial site (the PINK arrows in Figure-2).
  • As to ST-T wave changes in the 12-lead ECG — although some leads show T wave inversion (ie, in leads III, V3 and V4) — I did not think this looked acute in this 30-year old man without chest pain.

Figure-2: I’ve labeled atrial activity from Figure-1 with colored arrows.


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What about the Repeat ECG?
A little later — this patient's ECG was repeated (Figure-3).
  • How would YOU interpret ECG #2 (that is shown in Figure-3)?

Figure-3: The 2nd ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio)


MY Thoughts on the ECG in Figure-3:
The repeat ECG is as challenging to interpret, as was the initial tracing. Fortunately, the simultaneously-recorded long-lead rhythm strip at the bottom of ECG #2 — once again allows us to determine the etiology of the beats with a different QRS morphology.
  • It also helps to know that in ECG #1 that was recorded a little earlier from the same patient (shown above in Figure-1) — the underlying rhythm was sinus bradycardia and arrhyhmia, with QRS widening due to RBBB — in which both junctional and ventricular escape beats were seen when the heart rate dropped below 50/minute. 


Putting both ECGs in Today's Case together:
To facilitate comparison — I've put both ECGs in today's case together in Figure-4. Once again, for ECG #2labeling P waves greatly facilitates identifying ECG features:
  • Sinus P waves in the repeat ECG are slow and irregular (RED arrows in the long lead II rhythm strip shown in the lower tracing in Figure-4).
  • Beats #3 and #4 in ECG #2 — are sinus-conducted beats with RBBB (with the same shape upright P waves, the same consistent PR interval, and the same QRS morphology as was seen for beats #1,2,3,4; 7,8 in the long lead II rhythm strip of ECG #1).

  • Beat #6 in ECG #2 is also sinus-conducted — but the PR interval before beat #7 is too short to conduct. This tells us that beat #7 in ECG #2 must be a junctional escape beat.
  • Similarly — beat #5 in ECG #2 is wide, manifests RBBB morphology, and is not preceded by any P wave — which defines beat #5 as another junctional escape beat.

  • Note that a small amplitude negative deflection is seen after the T wave of beat #7 (PINK arrows in simultaneously-recorded leads V5,V6 and the long lead II from ECG #2). As was the case in ECG #1 — since this PINK arrow negative deflection is not followed by a QRS complex, it represents a non-conducted, non-sinus P wave.

  • This leaves us with beats #1, 2 and 8. Note in the long lead II rhythm strip in ECG #2 — that none of these beats is preceded by a sinus P wave with a normal PR interval (a sinus P wave occurs just after the QRS of beat #1 — just before the QRS of beat #2, with a PR interval too short to conduct — and no sinus P wave at all is seen in the vicinity of beat #8).
  • A look at simultaneously-recorded leads I and III for beats #1 and 2 (and simultaneously-recorded leads V4,5,6 for beat #8)confirms that these non-conducting QRS complexes are wide and very different in morphology from the other beats in this tracing that show RBBB conduction. This tells us that beats #1,2 and 8 must be ventricular escape beats.

IMPRESSION: Both ECGs in today's case manifest similar features of marked sinus bradycardia and arrhythmia — underlying RBBB — junctional and ventricular escape beats when the heart rate slows — and some non-sinus, non-conducted P waves (the PINK arrow P waves seen in both ECGs).

Figure-4: Comparison between the 2 ECGs in today's case.


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Laddergram Illustration:
To better illustrate the mechanism of the 2 ECGs in today's case — I've drawn laddergrams in Figure-5 for each of the long lead II rhythm strips.

Figure-5: Laddergram illustration for the rhythm in today's case.


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How do these ECGs "Fit" with the Clinical Scenario?
Before going further — I will offer the following quote from Dr. Harry Mond: "Today's ECGs would be impossible to understand unless we understand the eccentricities of vagal hypertonia".
  • In my ECG Blog #61 — I addressed the issue of vagotonic block.
  • For the interested reader wanting to know more — I highly recommend review of the October 1, 2021 post in Dr. Mond's CardioScan — in which Dr. Mond covers "the ECG Spectrum of Vagal Hypertonia", with a fascinating series of vagotonia examples in otherwise healthy individuals.
  • CAVEAT: Although many of these rhythms are seen in seemingly healthy individuals — these are not always benign arrhythmias. 

Regarding Today's CASE:
The patient in today's case was a previously healthy 30-year old man — in whom the above 2 ECGs were recorded as part of a "routine" pre-employment physical.
  • When questioned — this patient acknowledged a few episodes of "dizziness", but no syncope. As a result, both the patient and medical provider were surprised by what these ECGs revealed.

My Thoughts on Seeing this Case:
  • Is the patient an endurance athlete? (who might therefore be predisposed to bradycardia and the training effect of increased vagal tone).
  • Did the patient have some form of underlying heart disease?
  • Was there a family history of sudden death or significant arrhythmia?

Suggested Evaluation:

  • Echo and Cardiac MRI (Looking for underlying heart disease and assessing for LV function).
  • ETT (Exercise Treadmill Test) — to see what happens to this patient's heart rate and how he handles progressively increasing levels of exercise.
  • Cardiac Monitoring over ~48 Hours — to quantify and qualify the severity and duration of bradycardia and its correlation with symptoms (as well as to see if there were any prolonged pauses).
  • LAB — including electrolytes, renal function, thyroid studies, etc.


CASE Follow-Up:

  • Additional History: The patient used to play soccer — but has not engaged in endurance activities with any regularity for the past 8 years.
  • Negative family history for sudden death or arrhythmia.
  • No suggestion of sleep apnea.
  • Echo — completely normal.
  • ETT — excellent level of activity and heart rate response to exercise. No evidence of ischemia.


CASE Disposition:

Opinions of consulting cardiologists on this case were divided. Many favored pacemaker implantation at this time. But the question remained — Could this all simply be a result of "Vagal Hypertonia?"

  • Ultimately (with completely informed patient consent) — the decision was made to implant a pacemaker. Pacing parameters were selected to encourage the patient's own rhythm. 


My Review of the Literature:

There is no perfect answer to the above questions. 

  • Although the patient had not engaged in regular endurance training for a period of years — his arrhythmias could simply be the result of "Vagal Hypertonia".
  • The diagnosis of enhanced vagal tone has to be a "diagnosis of exclusion" (ie, after ruling out underlying heart disease and/or a potentially "fixable" cause).
  • What concerned me most about the patient's ECGs was the presence of non-conducted P waves (that should have been conducted). That said — vagotonic block can do this! (as per ECG Blog #61 and Dr. Mond's Vagotonia Review). 
  • That said — enhanced vagotonia is not necessarily benign, as it can be one of the mechanisms for PAVB (Paroxysmal AtrioVentricular Block) — that can be potentially lethal (See the ADDENDUM in my ECG Blog #419 for detailed discussion of PAVB).
  • The mechanisms associated with vagotonia and vasovagal-induced syncope are complex — involving a complex interplay between parasympathetic and compensatory sympathetic nervous system responses. These responses become even more complex in younger adults, especially when associated with endurance activity (Gopinathannair et al — Arrhythm & Electrophys Rev 7(2):95-102, 2018).

  • BOTTOM Line: Some patients with worrisome bradyarrhythmias due to intermittent or persistent enhanced vagal tone at some point do need permanent pacing. Unfortunately, there is no good medication for treatment of vagal hypertonia. There is research on attempting cardio-vagal nerve denervation — but this remains controversial, and not a perfect solution (Cai et al — Front Physiol 14:1088881, 2023). And — this patient is symptomatic (ie, with "dizziness" on a number of occasions).



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Acknowledgment: My appreciation to ضياء كمال (from Zagazig, Egypt) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

  • ECG Blog #185 — My Ps, Qs, 3R System for Rhythm Interpretation.
  • ECG Blog #188 — Reviews how to read and draw Laddergrams (with LINKS to more than 100 laddergram cases — many with step-by-step sequential illustration).
  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
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Saturday, September 28, 2024

ECG Blog #449 — Isorhythmic AV Dissociation?


The ECG in Figure-1 — was obtained from a 45-year old man with diabetes, who was being treated for septic shock.


QUESTIONS:
  • How would YOU interpret the ECG in Figure-1?
  • What is the rhythm?
  • Why does QRS morphology in the long lead II rhythm strip change every-other-beat?

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


MY Thoughts on the ECG in Figure-1:
This is a challenging ECG to interpret because of: i) the changing QRS morphology; and, ii) the difficulty in seeing all of the P waves. That said — I was able to determine the rhythm within seconds because of the following observations:
  • All beats on this ECG are supraventricular! The "beauty" of having a 12-lead tracing with a simultaneously-recorded long lead II rhythm strip — is that this allows us to view each of the 12 beats on this tracing in 3 other simultaneously-recorded leads. Doing so confirms that even though there are 2 distinct QRS morphologies in the long lead II rhythm strip (especially obvious in lead III) — the QRS is narrow in all 12 leads. Therefore — the rhythm is supraventricular!
  • There is group beating! (seen in Figure-1 in the form of a bigeminal rhythm, in which the same shorter — then the same longer R-R interval alternates throughout the tracing).
  • Regular P waves are present throughout the entire tracing. This KEY observation can be verified within seconds — simply by using calipers (See Figure-2).

Figure-2: I've added RED arrows to the initial ECG — showing that regular P waves are present throughout the entire tracing.


PEARL #1: The clinician who does not use calipers to interpret complex arrhythmias like today's tracing — will invariably take more time for their interpretation, only to discover that they will never be certain about the regularity of atrial activity.
  • To optimally assess atrial activity — I simply set my calipers to the P-P interval between any 2 consecutive P waves that I can clearly identify. For example, in Figure-2 — 2 consecutive P wave deflections are clearly seen to occur at the same place within each of the longer R-R intervals (so that I chose to set my calipers to the P-P interval between the 3rd and 4th RED arrows in Figure-2).
  • Once I set my calipers to this P-P interval — I was able to easily "walk out" regular P waves throughout the entire long lead II rhythm strip.
  • PEARL #2: The reason today's tracing is so challenging — is that every 3rd P wave is so well hidden within the T waves of every odd-numbered beat. This is where awareness of simultaneously-recorded leads may prove invaluable! Although we do not see every 3rd P wave in the long lead II rhythm strip (because these P waves are hidden within the T waves of beats #1,3,5,7,9 and 11) — we do see an "on-time" tiny negative deflection right after the 1st T wave in lead V1 (2nd RED arrow in lead V1). This confirms that P waves are hidden at a similar point in the T wave of all odd-numbered beats. Therefore — there is an underlying regular atrial rhythm, with sinus P waves at ~110/minute.

PEARL #3: Today's rhythm does not represent complete AV block (and it does not represent isorhythmic AV dissociation). We can quickly determine this by focusing our attention on the PR interval just before the QRS complex of each beat that ends each of the longer R-R intervals (ie, the PR interval before beats #3,5,7,9 and 11).
  • Labeling P waves (as we have done with RED arrows in Figure-2) — greatly facilitates this process — and expedites us being able to tell that although the PR interval before beats #1,3,5,7,9 and 11 is slightly prolonged (ie, ~0.22 second) — this PR interval in front of all odd-numbered beats remains constant! Therefore — there clearly is at least some conduction.
  • PEARL #4: Despite the finding of a regular atrial rhythm — there are more P waves than QRS complexes (ie, there are 18 RED arrow P waves in Figure-2 — but only 12 QRS complexes). This means that some form of 2nd-degree AV block must be present — since not all P waves are being conducted to the ventricles.

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PEARL #5: At this point in my interpretation — I was virtually certain that today's rhythm represented some form of AV Wenckebach (ie, 2nd-degree AV block of the Mobitz I Type) — because of the information the above-described 5 Observations told me:
  • Observation-1: The QRS complex for all beats in all 12 leads of Figure-2 is narrow. Therefore — today's rhythm is supraventricular.
  • Observation-2: There is group beating (in the form of alternating longer-then-shorter R-R intervals). The presence of "group beating" should always raise the possibility of Wenckebach conduction — IF certain other features are also present.
  • Observation-3: The underlying atrial rhythm is regular (RED arrows in Figure-2). Knowing there is a regular sinus rhythm rules out the non-Wenckebach causes of group beating, such as atrial bigeminy.
  • Observation-4: At least some beats are being conducted to the ventricles (because the PR interval is constant before all of the beats that end longer R-R intervals). As per PEARL #3 — since at least some P waves are being conducted to the ventricles — this rules out 3rd-degree (complete) AV block!
  • Observation-5: There are more P waves than QRS complexes. This means that some of the regularly-occurring sinus P waves are not being conducted (which means some form of 2nd-degree AV block must be present).

MY Impression of ECG #1:
The above 5 Observations confer ECG features that characterize "the Footprints of Wenckebach!" — which is why within seconds of seeing today's ECG, I was virtually certain there was some form of 2nd-degree AV Wenckebach (See ECG Blog #164 — ECG Blog #55 ECG Blog #347and ECG Blog #154).
  • That said — I had not yet demonstrated cycles with progressive increase in the PR interval until an on-time sinus P wave is dropped (as should be seen with typical AV Wenckebach).

For Practical Purposes: I would be happy IF you stopped at this point, knowing that the above 5 observations make it virtually certain that today's rhythm represents 2nd-degree AV block of the Mobitz I Type ( = AV Wenckebach).
  • Beyond-the-Core: Take a LOOK at Figure-3 — in which I have used 3 colors to label a certain P wave pattern in this tracing that repeats itself over the 12 beats in the long lead II rhythm strip. What does each color signify?

Figure-3: I've used 3 colors to label all P waves in today's rhythm. What does each color signify?


The Colors in Figure-3:
It's easiest to break down what is happening in Figure-3 — by starting with the RED arrow P waves.
  • As noted above in Observation-4 — the RED arrow P waves in Figure-3 all manifest the same 0.22 second PR interval. Therefore — beats #1,3,5,7,9 and 11 are all conducted with 1st-degree AV block.
  • IF the rhythm in Figure-3 is AV Wenckebach — then either the PINK or the YELLOW arrow P waves must not be conducted. Doesn't it seem more logical for the YELLOW arrow P waves to be non-conducted? (which would mean that the PINK arrow P waves would be conducting beats #2,4,6,8,10 and 12 with a very long PR interval of ~0.38 second).

PEARL #6: The last 2 features to explain regarding today's ECG are: i) Why QRS morphology changes slightly with every-other-beat; and, ii) What the rest of today's 12-lead ECG shows.
  • Since we know that all beats in today's tracing are supraventricular (Observation-1 in PEARL #5) — and since all QRS complexes are conducted — the reason for slight change in QRS morphology every-other-beat must be the result of some aberrant conduction. As explained in ECG Blog #211 — whether a beat does or does not conduct with some aberration depends on the interplay between coupling intervals and the preceding R-R interval. Although I do not see a specific form of conduction delay in the slightly wider QRS complexes (which are the odd-numbered beats) — the differing R-R intervals most probably accounts for the aberrant conduction.
  • Mobitz I 2nd-degree AV block is commonly seen in association with acute or recent inferior and/or posterior infarction. That said — I thought ST-T wave appearance in the rest of the 12-lead ECG showed nonspecific (nondiagnostic) abnormalities. I did not see evidence on this tracing for recent or acute MI (but it is always important to look for ECG signs of recent inferior and/or posterior MI whenever you encounter Mobitz I 2nd-degree AV block).


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Laddergram Illustration:
The BEST way to prove that today's rhythm is 2nd-degree AV block of the Mobitz I (AV Wenckebach) Type — is to construct a laddergram, which I illustrate step-by-step in Figures-4 thru -10.


Figure-4: I find the easiest 1st step in drawing a laddergram is to complete the Atrial Tier, that shows atrial activity.



Figure-5: I next fill in the Ventricular Tier — which corresponds to the timing of those ventricular beats I am sure about. Since we know in today's tracing that all 12 beats are supraventricular — I drew the arrow for each of these QRS complexes in the Ventricular Tier facing downward (representing normal conduction of supraventricular impulses through the ventricles).



Figure-6: We are now ready to begin solving the laddergram. I do this by connecting those P waves from the Atrial Tier — to those QRS complexes that I am certain each of these P waves is conducting to (BLUE lines that I've drawn within the AV Nodal Tier).



Figure-7: It seems logical that the next P waves to conduct to the ventricles are those that are highlighted by BLUE arrows in this Figure-7. It should now be easy to see that conduction of this 2nd P wave in each group takes a bit longer to be conducted, which is the principal characteristic of Wenckebach conduction (BLUE lines that I've drawn within the AV Nodal Tier).



Figure-8: By the process of elimination — this means that the remaining BLUE arrow P wave is not conducted (ie, there are no unconnected QRS complexes left). This therefore "completes" the laddergram — by the "butt end" that I've added to the remaining BLUE arrow P waves.



Figure-9: For clarity — I now labeled each of the P waves in the long lead II rhythm strip with the same colors that I used above in Figure-3.



Figure-10: Most of the time when I draw a laddergram — I use the same color for all lines in the illustration, as shown here.



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Acknowledgment: My appreciation to Vansh Verma (from New Delhi, India) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

  • ECG Blog #185 — My Ps, Qs, 3R System for Rhythm.
  • ECG Blog #188 — Reviews how to read and draw Laddergrams (with LINKS to more than 100 laddergram cases — many with step-by-step sequential illustration).
  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
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  • ECG Blog #192 — The Causes of AV Dissociation
  • ECG Blog #191 — AV Dissociation vs Complete AV Block.

  • ECG Blog #389 — ECG Blog #373 — for review of some cases that illustrate "AV block problem-solving".
  • ECG Blog #236 — for an ECG Video Pearl on the 3 Types of 2nd-degree AV block.
  • ECG Blog #344 — thoroughly reviews the Types of 2nd-degree AV block (Mobitz I vs Mobitz II vs 2:1 AV Block).

  • ECG Blog #267 — Reviews with step-by-step laddergrams, the derivation of a case of Mobitz I with more than a single possible explanation.
  • ECG Blog #164Step-by-Step laddergram of Mobitz I.

  • ECG Blog #195 — reviews Isorhythmic AV Dissociation.


 

 
ADDENDUM (10/2/2024)Based on Question by Akash
For those readers who enjoy the challenge of drawing laddergrams — I've decided to publish the Question sent to me from Akash (in the Comments below).
  • As I've often emphasized — there may on occasion be more than a single possible explanation for the mechanism of a given complex arrhythmia!
  • IF you are able to "draw" your theory for a potentially plausible mechanism — then consider yourself correct in proposing an alternative mechanism (in which case — the only way to verify which proposed mechanism is correct for the case at hand would be by EP study).
  • The reason I thought it worthwhile to publish the excellent question that Akash asks — is that it illustrates the problem-solving process for complex rhythms, in which I have to "play" with a few potentially plausible laddergram solutions until I am able to come up with one that works.

This is the question by Akash (that I copied from the Comments below):
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Hello Dr. Grauer!
Long time lurker (and learner) here, posting for the first time.
  • Could this be a 2:1 AV block?
  • The first P wave (labelled with a RED arrow in Figure 3) is conducted (albeit with a slightly prolonged PR interval).
  • The next P wave (the one hidden within the T wave = PINK arrow) is not conducted.
  • The QRS complex labelled beat #2 is a junctional escape beat.
  • The third P wave (YELLOW arrow) fails to conduct — because it finds the distal conduction system refractory (because of the junctional escape beat).
Is this a reasonable explanation of this rhythm? I’m sure I’m missing something, but am unsure what that is. Please throw light, Dr. Grauer!
Warm regards — Akash
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MY Reply to Akash:
Your question Akash is an excellent one — and I actually thought of the solution you propose when first working through this case.
  • The problem however — is that if the 2nd P wave (first YELLOW arrow in Figure-11) was non-conducted because of 2:1 AV block and if beat #2 was a junctional escape beat — this would mean that you are proposing an accelerated junctional escape rate (because the R-R interval before beat #2 that you are proposing is junctional = 3.7 large boxes — which corresponds to an accelerated junctional escape rate of ~81/minute).
  • And — this would mean that unless inhibited by a sinus-conducted beat — the next junctional escape beat would occur 3.7 large boxes later = where I placed the BLUE circle. But since the next sinus P wave is set to occur where the 3rd RED arrow occurs — we can see that this next junctional beat would prevent the 3rd sinus P wave from conducting .... (You'd have to propose "takeover" of the rhythm by an accelerated junctional rhythm — which I would not expect given the constant and reasonable PR interval before beats #1,3,5,7,9,11).

  • P.S.: Accelerated junctional rhythms and junctional tachycardia can occur — but they are relatively uncommon in adults unless there is some underlying cause (ie, ischemia, shock, electrolyte disorders, post-cardiac surgery, etc.).

BOTTOM Line: I thought it unlikely that there was 2:1 block with a "usurping" accelerated junctional rhythm. I also thought the laddergram that I derived in Figure-10 looked perfectly plausible for 2nd-degree AV Block, Mobitz Type I ( = AV Wenckebach).


Figure-11: Unsuccessful proposed laddergram (See above).