ECG Blog #550 — Guess the Clinical Setting

The ECG in Figure-1 was obtained from a middle-aged man who presented with CP (Chest Pain). I was asked for my thoughts on the rhythm.

QUESTIONS:

• What is the rhythm?
• How certain are you of your answer?
• What is the probable cause of this rhythm?

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

My Approach to Today's Tracing: 

We are at a distinct disadvantage in Figure-1 for determining the rhythm. This is because we only see 9 beats, and because we lack a long lead rhythm strip. Nevertheless, a number of deductions can confidently be made.

• PEARL #1: LIfe is easier — IF we simply number the beats (as I have done in Figure-2). Doing so allows us to talk intelligently with colleagues about what is going on (as well as making it easier for us to appreciate relationships between P waves and neighboring QRS complexes).

Take Another Look in Figure-2:

• HINT:  Look first at the chest leads ...

Figure-2: I've numbered the beats in today's tracing.

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What We See in Figure-2:

P waves are present in front of beats 7,8,9 (RED arrows in Figure-3):

• The P wave in front of beat #7 is clearly too short to be normally conducted to the ventricles. Thus, at least for this one beat #7 — there is AV dissociation (which simply means that the P wave in front of beat #7 is not completely conducting this QRS complex).

Figure-3: RED arrows highlight the presence of sinus P waves.

PEARL #2: Recognizing that the PR interval in front of beat #7 is too short to be a normal sinus-conducted beat is the KEY clue to today's rhythm — as it tells us that beat #7 must be a ventricular escape beat!

• In contrast — the QRS complex in front of beats #8 and 9 is narrow, very different-looking than the QRS of beats #7,8,9 — and, the PR interval in front of beats #8 and 9 is constant and long enough to be sinus-conducted (I measure the PR interval in front of beats #7,8 to be ≥0.13-0.14 — and the PR interval might be longer if we were to see P waves in lead II).
• This tells us that beats #5 and 6 must be ventricular escape beats at the slightly accelerated rate of ~55/minute (the R-R interval between beats #5-6 and 6-7 being between 5-to-6 large boxes). 
• 
  
• PEARL #3: If we focus our attention on lead V3 — Doesn't the QRST complex of beat 7 look slightly different than the QRST of beats #5 and 6? (At least in lead V3 — the QRS and T wave of beat #7 are a little less tall than for beats #5 and 6). This tells us that beat #7 is a fusion beat, and proves that beats #5 and 6 are ventricular in origin (See ECG Blog #128 — for more on fusion beats).
• NOTE: It makes sense that beat #7 is a fusion beat — because the PR interval in front of this beat is just a little bit shorter than the PR interval of the sinus-conducting P waves in front of beats #8 and 9 (as we'll see momentarily in the Laddergram in Figure-5).

PEARL #4: That beats #5 and 6 are ventricular escape beats — is supported by another look at QRST morphology of beats #1-thru-4 in the limb leads:

• Note in lead I — that the QRS complex begins with a very deep and wide Q wave! We virtually never see such a deep and wide initial negative deflection in left-sided lead I with normal sinus conduction. Thus, this initial deep and wide Q wave in lead I strongly suggests a ventricular etiology for the 4 beats in this lead.
• PEARL #5: Note the subtle-but-real negative deflection at the end of the QRS in each of the 3 inferior leads (YELLOW arrows in Figure-4 highlighting this negative deflection in lead III — but with a similar terminal negative deflection also being seen in leads II and aVF). This terminal negative notch most likely reflects retrograde conduction of the P wave from ventricular beats #1,2,3,4.
• I suspect retrograde conduction continues in the chest leads, and is seen after beats #5 and 6 — until slight acceleration of the underlying sinus P wave rhythm allows the RED arrow P waves in front of beats #8 and 9 to recapture the ventricles with sinus-conducted beats #8 and 9 (See the laddergram below in Figure-5). 

Figure-4: YELLOW arrows suggest retrograde conduction of P waves following ventricular escape beats.

Figure-5: Laddergram suggesting the mechanism of today’s rhythm.

My Impression: I suspect the rhythm in Figure-5 begins with 7 beats of AIVR (Accelerated IdioVentricular Rhythm) at ~55-60/minute — and ends with 2 sinus-capture beats ( = beats #8 and 9).

• The first 6 ventricular beats manifest retrograde P waves (dotted RED lines in the laddergram that are headed back to the atria).
• Slight acceleration of the rate of sinus impulses allows the RED arrow P waves to recapture the ventricles with beats #8 and 9.
• The overly short PR interval and intermediate shape of the QRS complex and of the T wave for beat #7 — suggests this is a fusion beat. Early arrival of this 1st RED arrow P wave in the ventricles prevents retrograde conduction of ventricular beat #7 — which therefore makes it possible for the 2nd RED arrow P wave to “capture” the ventricles with a sinus-conducted beat.

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Putting It All Together:

• Today’s patient presented with CP.
• The underlying rhythm in the initial ECG appears to be sinus bradycardia and arrhythmia that is intermittently interrupted by AIVR at a rate of ~55-60/minute.
• 
  
• PEARL #6: The combination of AIVR in a patient who presents to the ED for CP — is commonly seen during the evolution of an acute OMI ( = Occlusion-based Myocardial Infarction). As a result — We need to go back and Take Another LOOK at the initial ECG in today's case, looking to see if there might be subtle ECG clues of a recent OMI (keeping in mind that acute ST-T wave changes of an OMI may be difficult to recognize in the presence of a ventricular rhythm such as AIVR).

PEARL #7: When AIVR is seen in association with an evolving OMI (as is especially likely when the patient presents with CP, as in today's case) — it often represents a reperfusion arrhythmia (See ECG Blog #108 — for the basics regarding AIVR).

• As a result — correlating each serial ECG with the presence and severity of CP becomes especially important for understanding the sequence of events (and for determining whether the "culprit" artery is likely to be open or closed at the time a given ECG is recorded). 
• In today's case — We would want to find out IF this patient's CP had decreased (or resolved) at the time the initial ECG was recorded. If symptoms are less at the time of this initial ECG before any treatment has been administered — this would suggest that there has been spontaneous reperfusion of the "culprit" artery (in which case ECG signs of acute infarction may be especially subtle!).

In Figure-6 — I've reproduced today's initial ECG.

• Take another LOOK at this initial ECG — with special attention looking for subtle signs of recent infarction.

Figure-6: I've reproduced today's initial ECG.

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Subtle ECG Signs of Recent Infarction:

Despite the presence of AIVR (and the likelihood of sponaneous reperfusion) — I thought there are subtle ECG signs of recent infarction in today's initial ECG (See labeled Figure-7 below):

• I focused first on the 2 sinus-conducted beats — since assessment of ST-T waves for acute changes is more reliable when seen in normally conducted beats than it is when looking at ventricular beats ( = beats #8 and 9 — within the RED rectangle in Figure-7).
• The amount of ST elevation in lead V2 for beats #8,9 looks to be disproportionately increased given modest depth of the S wave in these sinus-conducted beats.
• The ST segment takeoff in lead V3 looks to be straightened for sinus-conducted beats #8,9.
• There is ST segment straightening with slight depression in lateral chest lead V6 (BLUE arrow in this lead).   

To Emphasize: Acute ST-T wave changes can sometimes be seen in ventricular beats. It's just that these changes tend to be subtle and more difficult to recognize than when acute changes are seen in normally conducted beats:

• In the limb leads (which show 4 consecutive ventricular beats) — the overly "bulky" and depressed ST-T waves in each of the inferior leads looks disproportionate and "off" for what I'd expect given modest QRS amplitude in leads II,III,aVF (RED arrows in these leads).
• Given this inferior lead ST-T wave appearance — the elevated and overly large upright T waves in leads I and aVL manifest the mirror-image opposite picture of what we see in the inferior leads (BLUE arrows in leads I and aVL).
• In the chest leads — the ST-T wave in lead V2 looks to be disproportionately large, with an angled and overly elevated J-point for the ventricular beats. Especially in leads V4,V5,V6 — the T waves look disproportionately large given the tiny size of the QRS in these lateral chest leads (RED arrows in the above noted chest leads for ventricular beats #5,6,7).

Impression: The above noted subtle signs in multiple leads of Figure-7 in this patient with CP and intermittent AIVR are suggestive of a Precordial "Swirl" pattern from recent acute LAD occlusion (See ECG Blog #380 — for review of Precordial Swirl).

• To Emphasize: The above ECG findings are subtle! But especially IF this patient's CP was less (or resolved) at the time the ECG in Figure-7 was recorded — we are expecting less obvious ECG signs than what would probably have been seen if severe CP was still present.

Figure-7: I've labeled a series of subtle ST-T wave abnormalities present in Figure-6 that suggest there has been a recent OMI.

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The CASE Concludes:

Providers were appropriately concerned by this patient's history of new CP in association in association with today's initial ECG.

• Cardiac cath was performed in a timely manner — and revealed acute proximal LAD occlusion, amenable to PCI. 
• A repeat ECG done the next day after successful PCI is shown below in Figure-8.

QUESTIONS:

• How do you interpret the repeat ECG in Figure-8?
• How do beats #8 and 9 in ECG #2 compare with beats #8 and 9 in Figure-7?
• Why might the voltage be so low in Figure-8?

Figure-8: Repeat ECG done the day after successful PCI.

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ANSWERS:

AIVR has resolved — with reestablishment of a sinus rhythm in the repeat ECG recorded after successful PCI (RED arrows showing sinus bradycardia at ~55/minute throughout the tracing in Figure-9).

• Note that all 5 sinus-conducted beats in the chest leads of this repeat ECG look identical to sinus-conducted beats #8 and 9 in today's initial ECG.
• Note that the QRS in Figure-9 is now narrow in all beats — whereas the QRS was wide for the ventricular beats in Figure-6. The wide initial Q wave in lead I that tipped us off in the initial ECG to the presence of AIVR is no longer present.
• There is poor R wave progression in the chest leads of Figure-6 (a QS is present in leads V1,V2 — and transition to a predominant R wave never occurs). This is consistent with this patient's recent anterior MI.
• This post-PCI tracing is also remarkable for diffuse low voltage (No R wave exceeding 5 mm in the limb leads — with overall reduced QRS amplitude also in the chest leads). As highlighted in other cases on this ECG Blog — the finding of low voltage in a patient with recent infarction may be a sign of myocardial "stunning", with reduced cardiac output (See ECG Blog #272 — for more on the causes of low voltage).

Figure-9: I've labeled sinus P waves in the repeat ECG.

Final Thoughts:  

Common things are common. Recognition of AIVR in a patient who presents with CP is an important clue to the likelihood of recent infarction. This should prompt:

• Attention to the details of the patient's history — with efforts to closely correlate the presence and relative severity of CP to the timing of each ECG. Recognition of AIVR at a time when the patient's CP has decreased or resolved is an important clue that spontaneous reperfusion may have occurred.
• ECG signs of recent infarction may be especially subtle following spontaneous reperfusion — as was probably the case for today's initial ECG.
• The ECG signs of recent infarction in Figure-7 are admittedly subtle! That said — these subtle signs become much easier to recognize when you know that the combination of CP and AIVR is commonly seen following recent infarction (and when you know that ECG clues may be very subtle if the patient's CP has decreased or resolved at the time the initial ECG was recorded).

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Acknowledgment: My appreciation to Ali Ibrahim (from Tikrit, Iraq) for allowing me to use this case and these tracings. 

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ECG Blog #549 — No Chest Pain

The ECG in Figure-1 is from a middle aged woman who presented with palpitations and dizziness of 2 hours duration. No chest pain. BP ~120/70 mm Hg.

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

QUESTIONS: 

• How would you interpret the ECG in Figure-1?
• Do the wide beats represent NSVT (Non-Sustained Ventricular Tachycardia) — or aberrant conduction?
• How certain are you of your answer? 
• What would you do?
• Does this ECG show anything else?

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DISCLAIMER:

My follow-up of the above case is unfortunately limited. That said — What counts is your approach to this arrhythmia. 

• This matches the clinical reality that we so often encounter — that is, seeing a patient for whom we need to initiate management before we know for certain what the diagnosis is.

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I've numbered the beats in Figure-2.

Take Another LOOK at this ECG ...

• What are the hints in this tracing that either point to the likelihood of VT? — vs suggesting that the wide beats are aberrantly conducted?

Figure-2: I've numbered the beats in today's tracing.

MY APPROACH:

The simple step of numbering the beats is surprisingly helpful!

• Numbering the beats instantly allows better appreciation of the relationship between the elements of a complex tracing.
• It also allows you to intelligently discuss the case with others (Since otherwise, valuable time will inevitably be lost trying to figure out which beat(s) is being discussed).
• NOTE: We lack a long lead rhythm strip in today's case. If I was seeing this patient in real time — I would immediately record a period of ongoing monitoring in a long lead II, since otherwise there is no way to know for sure IF the frequent changes in QRS shape that we see in the 12-lead tracing are the result of a single QRS morphology or multiple QRS morphologies arising from multiple sites in the ventricles.

My Observations:

The "good news" — is that although today's patient is symptomatic (ie, with palpitations and dizzyness) — she appears to be at least relatively hemodynamically stable (ie, without chest pain — in association with a BP = 120/70 mm Hg). This leaves us with at least a moment of time to try to determine — What is the underlying rhythm?

• To answer this question — I focused my attention on the narrow beats in Figure-2. These are beats #7,8,9; 11,12,13; 15,16,17; and 23,24,25.
• Note that no P waves are seen anywhere in Figure-2 (ie, Although we see multiple small undulations in the baseline — We do not see any with a consistent enough shape to verify as truly being P waves).
• Note also that the overall heart rate of the narrow beats in this tracing is fast — with a constantly changing R-R interval that is less than 3 large boxes in duration ( ==> the average ventricular rate is over 100/minute). 
• Impression: The underlying rhythm in today's tracing, as suggested by the irregularly irregular narrow QRS complexes without convincing indication of true P waves in Figure-2 — appears to be AFib (Atrial Fibrillation), here with a rapid ventricular response.

I next focused my attention on the wide beats:   

• Note that despite the underlying rhythm of AFib — the coupling interval of wide beats in this tracing remains the same! (ie, The distance from the narrow beat that precedes wide beats #10,14,18,26 is constant — as highlighted below by the 4 "C's" in Figure-3). 
• Given that the underlying rhythm in today's tracing is AFib — Shouldn't we expect the coupling interval to be as irregular as the underlying rhythm? (In contrast, with premature ventricular beats — the reentry mechanism that is most often operative with a single ventricular focus typically results in a constant coupling interval). 
• In addition — a post-ectopic pause (labeled "P") occurs after the 2 short runs of wide beats in Figure-3 (and a post-ectopic pause is clearly more likely to be seen after a run of ventricular beats compared to aberrantly conducted beats when the rhythm is AFib — since a run of wide beats with aberration tends to maintain a similar degree of irregularity as the underlying AFib).
• Finally — QRS morphology for the wide beats in Figure-3 is atypical for LBBB conduction, in that a predominantly positive QRS complex is already seen by lead V3, whereas normally — transition in the chest leads (ie, the point where the R wave becomes taller than the S wave is deep) does not occur until lead V5 or V6 when there is LBBB conduction.
• NOTE: QRS widening in Figure-3 does not manifest the Ashman phenomenon. This is because with the Ashman phenomenon — QRS widening from aberrant conduction follows a longer pause that predisposes to subsequent aberrant conduction by lengthening the subsequent relative refractory period. This is not what we see before beats #10,14,18 — which are not preceded by a relatively longer pause (See ECG Blog #70 and ECG Blog #71 — for review of the Ashman phenomenon).   

Clinical Impression:

• From a statistical viewpoint with rapid AFib — Intermittent QRS widening from aberrant conduction occurs much more commonly than ventricular ectopy. That said — the combination of constant coupling intervals, post-ectopic pauses after runs of wide beats, and a QRS morphology for the wide beats that is atypical for LBBB conduction — all favor ventricular ectopy as the cause of intermittent QRS widening.
• If the wide beats are of ventricular etiology — then the runs of 6 and then 5 consecutive wide beats ( = beats #1-thru-6 — and then #18-thru-22) constitute runs of NSVT. That said — since we do not see what happened before beat #1 in Figure-3 — We have no idea as to how long the 1st run of wide beats really lasts? 
• P.S.: QRS morphology during the runs of wide beats suggest that this is RVOT VT (Right Ventricular Outflow Track VT) — because QRS morphology resembles lbbb conduction in the chest leads in association with a rightward frontal plane axis (See ECG Blog #525 — for more on RVOT VT).

Figure-3: I’ve labeled findings suggestive of ventricular ectopy.

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What is the Cause of NSVT in today’s Case?

After assessment of a complex rhythm — it’s important to Take Another LOOK at the 12-lead ECG in search of potential clues that might explain the cause of the rhythm.

• In the absence of more information (and a prior ECG) — We do not know if the AFib in today’s case is new or old? Presumably (given the patient's new symptoms of palpitations and dizzyness) — the runs of NSVT are most likely new.

QUESTION:

• Do you see any potential clues in Figure-3  — as to what might be causing the runs of NSVT?
• HINT: Look closely at ST-T waves in the chest leads.

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A Hint suggesting the Cause …

I highlight in Figure-4 — a hint to the cause of the runs of NSVT.

• For assessment of ST-T wave morphology — it’s best to focus attention on the normally conducted ( = narrow) beats.
• ST-T waves in narrow beats #7,8,9; 11,12,13; and 15 — show nonspecific ST-T wave flattening.
• However, in the chest leads — there appears to be maximal ST depression in leads V3,V4,V5 (BLUE arrows in these leads).

Impression: Common things are common. 

• As is often emphasized on this ECG Blog — the finding of maximal ST depression in leads V2, V3 and/or V4 in patient with new symptoms may be the result of posterior OMI.
• And — an acute MI makes for a common setting that may precipitate runs of NSVT.
• Clearly — We can not prove that the precipitating cause of these runs of wide beats is an acute OMI, but our index of suspicion has to be raised (ie, with need to follow this patient with serial Troponins and repeat ECGs to see if this maximal ST depression in leads V3,V4,V5 persists once the rate of this patient's rapid AFib is controlled).

Figure-4: BLUE arrows highlight maximal ST depression in leads V3,V4,V5.

The CASE Concludes ...

Unfortunately my follow-up is limited beyond learning that sinus rhythm was restored with administration of IV Amiodarone — and maintained with beta-blockers without return of the runs of wide beats. 

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Acknowledgment: My appreciation for the anonymous contribution of today's case. 

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ECG Blog #548 — More than One "Family"?

I was sent the ECG shown in Figure-1. I was told that the patient had "palpitations", but was hemodynamically stable. Her admission diagnosis was DKA (Diabetic KetoAcidosis).

QUESTIONS:

• How do you interpret the ECG that is shown in Figure-1?
• Can you explain the rhythm?

A

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

My "Quick" ( = Initial) Impression:

Unfortunately, the information I was provided on this patient is limited. Nevertheless — I found a number of features in this initial ECG to be fascinating and worthy of discussion. Below my initial "quick thoughts" on Figure-1:

• The QRS is wide with a morphology consistent with RBBB (Right Bundle Branch Block) conduction (ie, predominant positivity in lead V1 — with wide terminal S waves in lateral leads I and V6).
• P waves are present in the long lead II rhythm strip — and without yet measuring, they appear to be at least fairly regular. And at least in front of beats #2,4,6,8 — the PR interval appears to be fixed and normal (therefore indicating at least some sinus conduction, as well as confirming that the rhythm is supraventricular with RBBB conduction).
• PEARL #1: There is group beating! (in the form of repetitive shorter-then-longer R-R intervals). When group beating is seen in association with a regular (or at least almost regular) P wave rhythm in which there is at least some sinus conduction — this suggests some form of Wenckebach conduction.

Turning my attention now back to QRS morphology:

• The QRS complex in leads V1 and V2 begins with a wide Q wave. Whether this Q wave is the result of previous infarction, pulmonary hypertension, or simply represents a less typical RBBB morphology is uncertain. But it’s worthwhile to be aware that the characteristic triphasic rsR’ of RBBB in lead V1 is for whatever reason, not seen in today’s tracing (therefore potentially worthy of follow-up as we learn more about the case).
• The T wave in lead V1, and in other anterior leads is upright in association with RBBB conduction. As reviewed in ECG Blog #204 (See the ECG Video and the Addendum in this ECG Blog #204) — normally with RBBB conduction, the ST-T wave should be oppositely directed to the last QRS deflection in lead V1 (and much of the time, also in other anterior leads).
• Instead — the T waves are surprisingly tall and peaked in leads V2,3,4 in this patient who presents with DKA! 
• PEARL #2: Acute acidosis is notorious for increasing extracellular serum K+ values ==> We need to find out the serum K+ level! (ie, One wonders how tall and peaked the anterior T waves in Figure-1 might really have been if ECG changes of hyperkalemia are not being superimposed on the ST-T wave depression that we would otherwise expect with RBBB conduction).
• PEARL #3: As emphasized in ECG Blog #275 — "All bets are off" regarding arrhythmias (especially forms of AV block) in the presence of hyperkalemia — with the "good news" being that much (most) of the time, these hyperkalemia-induced arrhythmias resolve once serum K+ is corrected. 
• As a result, since today's patient is hemodynamically stable in association with the rhythm in Figure-1 — determining the precise etiology of this fascinating rhythm is far less important than treating the patient's DKA (with treatment of DKA having an excellent chance of restoring a normal sinus rhythm).

The above said — I thought it instructive to explore how to go about assessing today's complex arrhythmia.

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Looking Closer at Today's Rhythm:

As I often emphasize — the simple step of numbering the beats and labeling P waves is often of invaluable assistance for both determining if the atrial rhythm is in fact regular — and for facilitating determination as to whether P waves are (or are not) related to neighboring QRS complexes.

• RED arrows in the long lead II rhythm strip at the bottom of Figure-2 — confirm that an underlying sinus rhythm is present, albeit with a very slight variation in the P-P interval (ie, ventriculophasic sinus arrhythmia — that is so commonly seen in association with 2nd- and 3rd-degree AV blocks).
• NOTE: For practical purposes and simplicity — I'll refer to the atrial rhythm in this blog as "regular", realizing that there is slight variation in the P-P interval.

Figure-2: RED arrows highlight an underlying sinus mechanism, with no more than minimal variation in the P-P interval.

To facilitate looking even closer at the mechanism of today’s arrhythmia — I’ll focus on the long lead II rhythm strip (See Figure-3 below):

• As noted a moment ago — the P waves in front of beats #2,4,6,8 are all upright and manifest a constant PR interval of 0.16 second. This tells us that at least these even-numbered beats — are all sinus-conducted with a normal PR interval.

Figure-3: Focusing on the long lead II rhythm strip …

Surprisingly (as shown in Figure-4) — BLUE arrows highlighting the P waves in front of beats #3,5,7 also manifest a constant (albeit much longer) PR interval.

• This suggests that these BLUE arrow P waves (despite their long PR interval of 0.44 second) — are also in some way being conducted!
• Had the rhythm strip in Figure-4 been started a little bit earlier — it most probably would have shown another BLUE arrow P wave with a similar prolonged PR interval of 0.44 second occurring before beat #1.

Figure-4: Since the PR interval preceding beats #3,5,7 is constant — these QRS complexes must be conducted (albeit with a very long PR interval). 

This leaves us with the YELLOW arrow P waves that I highlight in Figure-5 — as the only P waves that have not yet been addressed.

• By the process of elimination (ie, since each of the 8 QRS complexes in Figure-5 have been accounted for) — these YELLOW arrow P waves can not possibly be conducting. 
• This defines today's rhythm as representing some form of 2nd-degree AV block — because some (but not all) of the “on time” sinus P waves are conducting — but others are not.
• That is, there are a total of 15 P waves in Figure-5.
• 7 of these P waves (highlighted by the RED and BLUE arrows) are conducting 7 of the QRS complexes in this figure ( = beats #2-thru-8).
• The remaining 8 P waves (highlighted by YELLOW arrows) — are not conducted.

Figure-5: The YELLOW arrow P waves are not conducted.

A Laddergram is needed …

Today’s rhythm is complex! This tracing provides an example of one of the few times in which although I immediately recognized the general mechanism of today’s rhythm — I need to devise a laddergram in order to prove my theory.

KEY Points: I want you to walk away with the following concepts:

• Although it takes time and practice to become comfortable drawing laddergrams — knowing how to draw laddergrams is not necessary for optimal clinical management.
• In contrast — Learning to read laddergrams is EASY (as I'll demonstrate momentarily) — and this can help in selecting optimal management options.
• For interested readers — I review how to read and draw laddergrams in ECG Blog #188 (where I provide over 140 examples of laddergrams — many with step-by-step analysis). 

The “Quick” Answer to Figure-5:

We’ve already established that today’s rhythm manifests a supraventricular rhythm with RBBB conduction, regular P waves and group beating in which a number of “on time” P waves are conducting — but other “on time” P waves are not conducting.

• This establishes the rhythm as some form of 2nd-degree AV block — with the group beating strongly suggesting some form of Wenckebach conduction.
• As implied in the title of this ECG Blog post — there is more than a single “family” of PR intervals that conduct to the ventricles. Specifically: 
• RED arrow P waves conduct with a normal PR. 
• BLUE arrow P waves conduct with a longer PR.
• 
  
• PEARL #4: The most logical explanation for why a large PR interval "increment" may exist between 2 "families" of constant PR intervals — is that there are dual AV Nodal pathways that alternate conduction of sinus impulses:
• RED arrow P waves conduct with a normal PR interval of 0.16 second.
• BLUE arrow P waves conduct with a prolonged PR interval of 0.44 second.

My proposed Laddergram …

What follows is my step-by-step derivation of this laddergram: 

Figure-6: It's easiest to begin by completing the Atrial Tier (as shown by the vertical GREEN arrows that mark the onset of P waves).

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Figure-7: It's usually easiest to then complete the Ventricular Tier (GREEN arrows marking the onset of each QRS).

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Figure-8: It's now time to begin "solving" the laddergram — by postulating which P waves are most likely to be conducting to which QRS complexes. Depending on the complexity of the laddergram — this may entail some "trial and error". I start by connecting those P waves that I am most certain about (in this case — the RED arrow P waves that conduct with a normal PR interval to beats #2,4,6,8).

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Figure-9: I next connected the BLUE arrow P waves to beats #3,5,7. Because of the large PR interval "increment" between RED and BLUE arrow P waves — I used light BLUE lines to represent conduction over the slower AV nodal pathway.

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Figure-10: If conduction of the BLUE arrow P waves to the ventricles is over the slower AV nodal pathway — this means that the faster AV nodal pathway must be blocked at this time (which I represent by RED butt ends within the AV Nodal Tier). 

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Figure-11: This means that when normal conduction of the RED arrow P waves is occurring over the faster AV nodal pathway — the slower AV nodal pathway must be blocked (which I represent by adding the BLUE butt ends within the AV Nodal Tier).
= = = = = = =
NOTE: This leaves us with the 8 YELLOW arrow P waves — none of which are conducting ...

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Figure-12: Since none of the YELLOW arrow P waves are conducting to the ventricles — I complete the laddergram by schematically representing with RED and BLUE butt ends that both AV nodal pathways are blocked at this time.
= = = = = = =
Impression: One possible explanation of the mechanism for today's rhythm is that there may be 3:1 AV block in the faster AV nodal pathway that alternates with 3:1 AV block + 1st-degree AV block in the slower AV nodal pathway.

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More than One Possibility ...

What follows below goes way beyond-the-Core!

• My purpose in presenting an alternative laddergram to the one that I just derived in Figure-12 — is to illustrate the principle that with complex arrhythmias — there will often be more than a single possible explanation! 
• Without EP (ElectroPhysiologic) study — it will be impossible to know for sure which explanation is correct.
• Knowing which explanation is the "correct" one is not important for optimal clinical management.
• Unless your goal is to "dive in" to the specifics of complex arrhythmia interpretation — there is no need to concern yourself with the "Hows" and "Whys" of drawing this alternative laddergram.
• For those readers interested in "diving in" — I offer an alternative laddergram that I feel is more likely than postulating the simultaneous 3:1 AV blocks in both AV nodal pathways that Figure-12 suggests.

What follows is my derivation of this alternative laddergram: 

Figure-13: We can begin with the foundation established in Figure-7 — in which all P waves and QRS complexes are noted in the Atrial and Ventricular Tiers. 

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Figure-14: This alternative laddergram is based on the premise that when consecutive non-conducted "on time" P waves are seen in association with group beating suggestive of Wenckebach conduction — that there may be more than a single level of Wenckebach conduction out of the AV Node. I've presented this complex arrhythmia concept a number of times in this ECG Blog (See ECG Blog #259 — for a brief Audio Pearl and step-by-step laddergram demonstration of this phenomenon).
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NOTE: I schematically represent the concept of dual-level AV block by drawing a BLACK dotted line within the AV Nodal Tier.

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Figure-15: I fully acknowledge that I tried several combinations before coming up with a plausible one that worked, which I show above. I postulate that over the faster AV nodal pathway — there is 2:1 block in the upper AV Nodal level — and then again 2:1 block in the lower AV Nodal level (RED butt ends in the upper and lower AV Nodal Tiers, respectively).

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Figure-16: This means that somehow, conduction to the ventricles of beats #1,3,5,7 must be occurring over the slower AV nodal pathway (BLUE arrows in the Ventricular Tier).

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Figure-17: I postulate that conduction of the BLUE arrow P wave makes it through both AV nodal levels — with retrograde conduction in the lower AV Nodal level preventing the YELLOW arrow P wave from passing through this lower AV Nodal level.

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Figure-18: If my Figure-17 is correctly drawn — then it would seem logical that conduction over the slower AV nodal pathway is blocked elsewhere in this rhythm strip (which I show in the next figure).

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Figure-19: I complete this alternative laddergram by schematically representing with RED and BLUE butt ends where AV nodal pathways are blocked throughout the rhythm strip.
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Impression: This alternative laddergram postulates that there is dual-level block out of the AV Node with alternating 2:1 block in dual AV nodal pathways.

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In Summary:

The "quick answer" to today's complex arrhythmia is that the presence of regular P waves with 2 "families" of conducting PR intervals with a large PR interval increment — in association with group beating — strongly suggests there are dual AV nodal pathways.

• In addition — the finding of consecutive "on time" P waves that fail to conduct suggests there may be dual-level Wenckebach block out of the AV Node.
• Construction of a laddergram that works supports my theory that this is a plausible mechanism for today's arrhythmia.
• 
  
• CASE Follow-Up: As noted — this patient had DKA. Serum K+ at the time she presented = 7.0 mEq/L. Treatment of her DKA (with correction of her hyperkalemia) resulted in restoration of normal sinus rhythm. Along the way — today's initial rhythm provides arrhythmia enthusiasts with a fascinating account of the likely mechanism for this complex conduction disturbance.

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Acknowledgment: My appreciation for the anonymous contribution of today's case. 

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