ECG Blog #344 — Mobitz I, Mobitz II or Neither?

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 — See ECG Blog #404 — for a Video presentation of this case!

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How would YOU interpret the lead II rhythm strip shown in Figure-1?

• Is the rhythm Mobitz I or Mobitz II 2nd-degree AV Block? 
• Or — Is it “something else”?

Figure-1: How would YOU interpret this lead II rhythm strip?

MY Initial Approach to the Rhythm in Figure-1:

Unfortunately — We are not provided with any history, nor with the 12-lead tracing for this patient. That said — the ECG in Figure-1 provides us with enough information to interpret the rhythm. As always — I favor the Ps, Qs, 3R Approach (See ECG Blog #185).

• PEARL #1: It does not matter in what sequence you look for the Ps, Qs and 3Rs — and I often vary the sequence I use depending on specifics of the tracing at hand. Most of the time when it looks like some form of AV block may be present (ie, because it seems like a number of on-time P waves that should conduct are not conducting) — I find it easiest to start by identifying P waves. The simple step of using calipers to “walk out” the atrial rhythm allows me to establish within a few seconds whether or not there is an underlying regular atrial rhythm (RED arrows in Figure-2). 

Figure-2: Using calipers — I marked out a regular atrial rhythm (RED arrows).

Applying the Ps, Qs and 3Rs to Today’s Rhythm:

• P Waves: As highlighted by the RED arrows in Figure-2 — the atrial rhythm is fairly regular with similar looking P waves that are upright in this lead II rhythm strip. There is therefore slight sinus arrhythmia — with an atrial rate that varies between ~85-95/minute.
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• PEARL #2: As is evident for many of the examples of AV block that have appeared in this ECG Blog — it is extremely common for there to be a “ventriculophasic" sinus arrhythmia in association with 2nd or 3rd degree AV block. Much of the time (as is the case in Figure-2) — the shorter P-P interval is the one that “sandwiches” a QRS complex (the theory being that perfusion improves following ventricular contraction — with resultant shortening by a slight amount the P-P interval that contains a QRS).
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• QRS Width: The QRS complex in Figure-2 looks narrow (ie, not more than 0.10 second = not more than half a large box in duration). 
• NOTE: In order to be 100% certain that the QRS is truly narrow — We would need to see a 12-lead ECG (since on occasion — a part of the QRS may lie on the baseline in the 1 lead that you are looking at). That said, for practical purposes — the very narrow appearance of all QRS complexes in Figure-2 suggests that more likely than not, the QRS is narrow. 

And the 3 Rs:

• Rate and Regularity of the Rhythm: It is good to keep in mind that when a 1:1 relationship between P waves and QRS complexes is not present — that we need to assess the “rate” and “regularity” of both the atrial and ventricular rhythms. In Figure-2 — after beat #2, the ventricular rhythm is fairly regular at a rate just under 50/minute. As already stated — the underlying atrial rhythm is a minimally irregular “ventriculophasic” sinus arrhythmia at between ~85-95/minute.
• Related? (ie, Are P waves “married” to the QRS?): To assess whether P waves are (or are not) related to neighboring QRS complexes — I look in front of each QRS complex on the tracing. The fact that each QRS complex in today’s tracing is preceded by a P wave — and the PR interval in front of most of these QRS complexes is the same — confirms that there is at least some conduction!

QUESTION: Note in Figure-3 — that I have labeled each of the P waves in today's tracing with letters. 

• Which of these P waves are definitely not conducted?
• Are you uncertain about any of the P waves in Figure-3?

Figure-3: I’ve labeled each of the P waves from Figure-2. Which P wave(s) would you say are definitely not conducted?

Which P Waves are Not Conducted?

• We have established that each of the P waves preceded by the same PR interval in Figure-3 — are conducted (ie, the P waves labeled a, d, f, h, j, l are all conducted).
• Note that the PR interval for each of these 6 P waves that we know are conducted — is prolonged (ie, to about 0.31 second in duration). As a result — an underlying 1st-degree AV block is present.
• Those P waves in Figure- 3 that we know are not conducted — are the ones that occur after a beat, but which are not then followed by a QRS (ie, P waves c, e, g, i and k are not conducted).
• This leaves us with P wave "b" — about which we might not yet know whether this P wave is (or is not) conducted — because the PR interval of "b" is different (longer) than the PR interval for the above beats that we know are conducted.

Putting It All Together:

Thus far — We have established the following:

• There is an underlying ventriculophasic sinus arrhythmia (RED arrows in Figure-3).
• The rhythm appears to be supraventricular (at least according to this single monitoring lead — the QRS looks to be narrow).
• Focusing on that part of the rhythm that we are certain about (ie, forgetting for the moment about beats #1 and 2 — and focusing on what happens beginning with beat #3 — it is only every-other-P-wave that is conducted). This defines the rhythm as some type of AV block!

PEARL #3: The KEY to recognizing that the rhythm in Figure-3 represents some type of AV block (instead of non-conducted PACs) — is that the atrial rhythm is regular (or at least almost regular).

• Note that we have ruled out complete (ie, 3rd-degree) AV block — because the constant PR interval proves that at least some beats are conducted.
• Therefore — starting with beat #3, there is 2nd-degree AV block with 2:1 AV conduction.

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NOTE: The above concepts are easier to visualize when illustrated by use of a laddergram. 

• Continuing to focus on what happens beginning with beat #3 — the laddergram in Figure-4 shows that every-other-P-wave is conducted to the ventricles. 
• P waves highlighted by WHITE arrows are blocked (they do not make it out of the AV node). 
• Thus, beginning with beat #3 — there is 2:1 AV block.

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Figure-4: Laddergram illustration of the rhythm in Figure-3. Focusing on the rhythm beginning with beat #3 — RED arrows after this point indicate P waves that are conducted to the ventricles (albeit with 1st-degree AV block). On-time P waves that do not make it out of the AV node are highlighted by WHITE arrows (NOTE: For review on how to read and/or draw laddergrams — Please check out ECG Blog #188).

PEARL #4: As reviewed in detail in the ADDENDUM below — there are 3 Types of 2nd-degree AV block. These are:

• Mobitz I, 2nd-degree AV block ( = AV Wenckebach) — in which the PR interval increases until a beat is dropped.
• Mobitz II — in which the PR interval remains constant for consecutively conducted beats until one or more beats are non-conducted.
• 2nd-degree with 2:1 AV block — in which because of the fact that we never see 2 consecutively conducted beats — We are not able to tell if the PR interval would lengthen before dropping a beat IF given the chance to do so.
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• BOTTOM Line: If the rhythm strip in Figure-4 began with beat #3 (and we only saw beats #3-thru-7) — then we would not be able to tell if this rhythm represents the Mobitz I or Mobitz II form of 2nd-degree AV block. KEY Point: Distinction between Mobitz I and Mobitz II is important — because the clinical course of Mobitz I is often fairly benign — whereas patients with Mobitz II are much more likely to need a permanent pacemaker.

PEARL #5: There are a number of ECG and clinical Clues that may help to determine IF the type of 2nd-degree AV block you are looking at is more likely to be a Mobitz I or Mobitz II block. These clues include the following:

• Mobitz II is rare. In my experience — well over 90-95% of all 2nd-degree AV blocks will turn out to be Mobitz I.
• The QRS complex will most often be wide with Mobitz II. In contrast — the QRS is most often narrow with Mobitz I (although an exception may exist if there is preexisting bundle branch block in a patient with Mobitz I).
• Mobitz I is most often associated with recent or acute inferior infarction. In contrast — Mobitz II is usually associated with anterior infarction.
• The PR interval of conducting beats with Mobitz I is often prolonged. In contrast — the PR interval of conducting beats with Mobitz II is often normal.
• Finally — It is unlikely to switch back-and-forth from Mobitz I to Mobitz II (or vice versa). Therefore, IF on reviewing additional monitoring on your patient you see clear evidence of Mobitz I (ie, progressive PR interval lengthening until a beat is dropped) — then it is very likely that the 2:1 AV block you are looking at also reflects Mobitz I.

Applying the Clues from PEARL #5:

Take one last look at the laddergram in Figure-4.

• QUESTION: What is happening at the beginning of this tracing?

ANSWER:

The completed laddergram in Figure-5 answers this question.

• The P wave in front of beat #1 in Figure-5 — is conducted with the same prolonged PR interval as is seen preceding conducted beats #3,4,5,6,7 (RED arrows).
• The P wave in front of beat #2 is also conducted (BLUE arrow) — but with a further increase in the PR interval.
• The WHITE arrow P wave seen after beat #2 is not conducted.
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• Putting It All Together: The first 2 beats in Figure-5 form a typical Wenckebach cycle (ie, progressive increase in the PR interval until a beat is dropped). This strongly suggests that the 2:1 AV block that begins with beat #3 also represents Mobitz I, 2nd-degree AV block. In support of this conclusion (as per Pearl #5) are: i) Statistics (ie, Mobitz I is so much more common than Mobitz II); ii) The narrow QRS complex for all beats in today's tracing; and, iii) The prolonged PR interval seen for all conducted beats.

Figure-5: I've completed the laddergram from Figure-4 (See text).

CASE Conclusion:

The above deductions illustrate how we arrive at a definitive diagnosis of 2nd-degree AV Block, Mobitz Type I with 3:2 and 2:1 AV conduction for today's tracing. Although I unfortunately lack specific follow-up for this case — We emphasize that clinical decision-making would be based on the following concepts.

• The overall ventricular rate in today's tracing is ~50/minute. At this overall heart rate — the patient may or may not be symptomatic. Symptoms may be subtle (ie, a vague "sense" of fatigue). Clearly, treatment recommendations will be greatly influenced by symptoms that result directly from bradycardia.
• The longterm prognosis of Mobitz I may be benign — especially if associated with recent inferior infarction that is successfully treated (ie, It is common for Mobitz I to spontaneously resolve in such patients over a period of days to 1-2 weeks).
• It is possible that this patient's conduction defect might improve IF — some other "fixable" precipitating factor(s) is present (ie, electrolyte disorder, sleep apnea, use of a rate-slowing medication). Permanent pacing will not be needed IF you can "find and fix" the precipitating cause of the rhythm.
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• On the other hand — If the degree of AV block progresses — or the ventricular rate slows more and/or the patient develops persistent bradycardia-related symptoms — then permanent pacing will be needed, even though the conduction defect is "only" Mobitz I.

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Acknowledgment: My appreciation to Hafiz Abdul Mannan Shahid (from Lahore, Pakistan) for the case and these tracings.

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ADDENDUM (11/13/2022):

• I've included below an Audio Pearl — a Video Pearl — and links for download of PDFs reviewing the ECG diagnosis of AV Blocks.

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ECG Media PEARL #4 (4:30 minutes Audio): — takes a brief look at the AV Blocks — and focuses on WHEN to suspect Mobitz I.

My GOAL in the 15-minute ECG Video below — is to clarify ECG diagnosis of the 2nd-Degree AV Blocks, of which there are 3 Types:

• Mobitz I ( = AV Wenckebach).
• Mobitz II.
• 2nd-Degree AV Block with 2:1 AV conduction.

This 15-minute ECG Video (Media PEARL #52) — Reviews the 3 Types of 2nd-Degree AV Block — plus — the hard-to-define term of "high-grade" AV block. I supplement this material with the following 2 PDF handouts.

• Section 2F (6 pages = the "short" Answer) from my ECG-2014 Pocket Brain book provides quick written review of the AV Blocks (This is a free download).
• Section 20 (54 pages = the "long" Answer) from my ACLS-2013-Arrhythmias Expanded Version provides detailed discussion of WHAT the AV Blocks are — and what they are not! (This is a free download).

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #185 — Review of the Ps, Qs, 3R Approach for systematic rhythm interpretation.
• ECG Blog #188 — Reviews how to read and draw Laddergrams (with LINKS to more than 50 laddergram cases — many with step-by-step sequential illustration).
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• ECG Blog #164 — Which reviews step-by-step the diagnosis of a Mobitz I 2nd-degree AV block (with sequential laddergram illustration).
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• ECG Blog #168 — A complex dual-level AV Wenckebach (Laddergram).
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• ECG Blog #154 and ECG Blog #55 and ECG Blog #224 and ECG Blog #232 — Acute MI with AV Wenckebach.
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• ECG Blog #63 — Mobitz I with Junctional Escape Beats.

ECG Blog #343 — GI Bleed and a "Funky" ECG

The 12-lead ECG with long lead II rhythm strip in Figure-1 — was obtained from a patient who was admitted for GI bleeding. She had a prior history of AFib and coronary disease. The patient had no cardiac symptoms — and, she was hemodynamically stable at the time this ECG was obtained. 

• How would YOU interpret the ECG in Figure-1?
• What is the rhythm?

Figure-1: 12-lead ECG and long lead II rhythm strip from a woman with a GI bleed. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Initial Thoughts on the ECG in Figure-1:

As always — I favor starting with the long lead rhythm strip before turning my attention to the 12-lead ECG. This approach is especially relevant for today's tracing — since determining the cardiac rhythm is essential for interpreting this tracing!

• A bigeminal rhythm is consistently seen throughout the long lead II rhythm strip shown in Figure-1. That is — we see "group" beating, in which QRS morphology alternates for the 2 beats in each pair.
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• PEARL #1: I've presented a variety of bigeminal rhythms in my ECG Blog (links to many of which I list at the bottom of this page). The etiology of some of these bigeminal rhythms can be deceptive — which is why awareness of the common differential diagnosis may be extremely helpful (Figure-3).

Figure-2: Common causes of a bigeminal rhythm.

A Closer Look at the Rhythm in ECG #1:

I've emphasized my use of the Ps, Qs, 3R Approach to rhythm interpretation (ECG Blog #185). Today's rhythm is one in which the KEY step after recognizing the group beating of a bigeminal rhythm — is to identify P waves.

• RED arrows in Figure-3 highlight P waves that are rapid and regular (at ~135/minute) throughout the entire tracing.

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NOTE: If you had trouble finding the P waves highlighted by RED arrows in Figure-3 — then you probably did not use calipers. The clinical realities are: 

• i) If you do not regularly use calipers for complex rhythms — then you will often miss the diagnosis! 
• ii) Once you get used to using calipers — You will find that it SAVES you a LOT of time (because you can instantly confirm or refute P-to-QRS relationships).

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QUESTIONS:

• Are any of these RED arrow P waves conducting to the ventricles?
• IF so — Which P waves are conducting?

Figure-3: I've highlighted sinus P waves with RED arrows.

Which P Waves are Conducting?

Interpretation of today's tracing is complicated by the fact — that the underlying rhythm is ATach (Atrial Tachycardia) at the rapid rate of ~135/minute.

• Note that the PR interval is constant and normal (ie, ~0.16 second) in front of all odd-numbered beats in Figure-3. As a result — it appears that the P waves in front of beats #1,3,5,7,9,11,13,15,17,19 and 21 are all being conducted to the ventricles.
• In contrast — the PR interval for all P waves in front of even-numbered beats are all too short to be normally conducted. While possible that there is some degree of fusion between supraventricular and ventricular impulses — the fact that the P waves in front of beats #2,4,6,8,10,12,14,16,18,20 and 22 occur so close to the QRS complex of these beats means that these beats have to be originating from below the AV node!
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• PEARL #2: It's impossible to tell from Figure-3 if even-numbered beats do (or do not) manifest some degree of fusion. This is because we never see an even-numbered beat that is not preceded by a P wave. As a result — we can not tell if QRS morphology for even-numbered beats in Figure-3 is the same as the QRS morphology would be for a pure ventricular beat.
• That said — Clinically, it does not matter if there is (or is not) fusion of even-numbered beats — because the fact that the PR interval in front of these beats is so short tells us that these beats have to be at least in part arising from the ventricles! (For more on the ECG diagnosis of Fusion Beats — Please check out ECG Blog #128).

QUESTION:

• Is the QRS complex wide or narrow for conducted beats in today's tracing?
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• HINT: How does Figure-4 help to answer this question?

Figure-4: To facilitate identifying which beats are wide and which are narrow — I've enclosed within RED-YELLOW rectangles simultaneously-recorded beats from each 3-lead grouping.

Is the QRS Wide or Narrow?

The "tricky" part of today's tracing — is that the QRS complex does not look very wide for any of the 22 beats in the long lead II rhythm strip. Fortunately — We can use the simultaneously-recorded leads in the 12-lead ECG (within the RED-YELLOW rectangles in Figure-4) — to facilitate assessment of which beats are wide, and which are narrow.

• Start by looking at simultaneously-recorded leads I,II,III for beat #4. The QRS complex of beat #4 looks to be obviously widened in leads I and III — but not so in lead II, because part of the QRS lies on the baseline in this lead.
• The QRS looks wide in leads aVR,aVL,aVF for beat #10.
• The QRS looks wide in leads V1,V2,V3 for beat #16
• But the QRS does not look wide in leads V4,V5,V6 for beat #20!

Putting It All Together: 

When assessing interval duration (of the PR, QRS or QTc intervals) — one uses the longest interval that can clearly be seen in any of the 12 leads. Therefore, despite the narrow appearance of even-numbered beats in the long lead II rhythm strip — simultaneously-recorded leads confirm that the QRS is wide for all even-numbered beats!

• Note that each of the even-numbered beats in Figure-4 are "premature" (ie, they occur slightly earlier-than-expected).
• QRS morphology for even-numbered beats in the chest leads — is potentially consistent with RBBB-conduction. That said — the qR configuration in lead V1 (ie, with taller left "rabbit ear" in this lead) is atypical. QRS morphology is even more atypical for supraventricular conduction in the limb leads, because the predominantly negative QRS in both leads I and II — with qR pattern in lead III — resembles neither LAHB nor LPHB conduction.
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• BOTTOM Line: I interpreted the rhythm in today's ECG as showing ATach at ~135/minute with ventricular bigeminy (ie, every-other beat a PVC). Note in Figure-2 — that ventricular bigeminy is one of the causes of a bigeminal rhythm.

CASE Conclusion: 

Now that we've interpreted the rhythm in today's case — We need to focus our attention on QRST morphology of the conducted beats in each of the 12 leads (ie, on odd-numbered beats #1, 3, 5, 7, 9, 11, 13, 15, 17, 19, 21).

• There is LAD (Left Axis Deviation) — with an all positive QRS in lead I for conducted beats — and predominant negativity in lead aVF for conducted beats. But there is not enough LAD to qualify as LAHB (Left Anterior HemiBlock) — because the QRS of beats #1,3,5 in lead II is more positive than negative (ie, the frontal plane axis is about -15 degrees).
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• There is LVH (ie, the R wave in lead aVL >12 mm — with ST-T wave changes of LV "strain" in high-lateral leads I and aVL).
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• Lead V2 may be malpositioned — as it does not make physiologic sense for the R wave of conducted beats in lead V2 to be taller than the R wave in both leads V1 and V3 — and it does not make physiologic sense for the T wave in V2 to be inverted when it is not inverted in either neighboring lead.
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• Transition (ie, where the R wave becomes taller than the S wave is deep) — is slightly delayed in this ECG (ie, it only occurs between leads V5-to-V6).
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• Finally — There is symmetric T wave inversion in the odd-numbered beats of most chest leads. This may be ischemic (and/or it may be related to the frequent ventricular ectopy).
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• FOLLOW-UP: Unfortunately, I do not know the hospital course of this patient. That said — there does not appear to be any sign of an acute cardiac event on ECG — nor any symptoms of pulmonary embolus. Highest priority for management would therefore entail control of this patient's GI bleed — with optimization of oxygenation, fluid status, and ensuring normal electrolytes. Hopefully — addressing these priorities will control the atrial rate, reduce the ventricular ectopy, and result in improvement of the chest lead T wave inversion. Close follow-up will clearly be needed.

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ADDENDUM (November 8, 2022):

• The Audio PEARL (5:45 minutes) below reviews the concept of Bigeminy.

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Acknowledgment: My appreciation to Abdullah Alhasan @EcgOxford (from Kuwait) 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 and 3R Approach to Systematic Rhythm Interpretation.

ECG Blog #232 — Reviews an example of a bigeminal rhythm.

ECG Blog #312 — Another example of a bigeminal rhythm.

ECG Blog #163 — Reviews a case of "escape-capture" bigeminy, in which SA block might be operative.

ECG Blog #256 — Reviews another case of "escape-capture" bigeminy (in which retrograde conduction from junctional escape results in "capture").

ECG Blog #33 — Reviews a case showing blocked and aberrantly-conducted PACs. 

ECG Blog #66 — Reviews a case showing blocked and aberrantly-conducted PACs. 

ECG Blog #147 — Reviews a case showing blocked PACs. 

ECG Blog #57 — Reviews a case showing atrial bigeminy with blocked PACs.

ECG Blog #128 — Reviews the concept of Fusion Beats.

ECG Blog #342 - This IS a 12-Lead ECG ...

The pre-hospital 12-lead ECG shown in Figure-1 — was obtained from an older woman complaining “odd heartbeat” episodes that began today. In between episodes — her heartbeat would return to normal.

• How would YOU interpret her ECG in Figure-1?
• What is the likely diagnosis? How would you confirm this?

Figure-1: The prehospital ECG of an older woman with episodes of “odd heartbeat”. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the ECG in Figure-1:

Although there is no long lead rhythm strip in Figure-1 — this patient’s problem is obvious from the 12-lead tracing.

• The QRS is narrow for the first 6 beats in this tracing (beats #1-thru-5 in simultaneously-recorded leads I,II,III — and the 6th beat recorded in leads aVR,aVL,aVF). The rhythm for these 6 beats is fast (over 100/minute) — and irregularly irregular without P waves. This defines the rhythm for these first 6 beats as AFib (Atrial Fibrillation) with a rapid ventricular response.
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• An extended pause follows the 6th QRS complex. The duration of this pause is over 24 large boxes ( = almost 5 seconds!). Finally — a beat occurs ( = beat #7 in Figure-2).
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• Beat #7 is probably conducted — because this beat is preceded by a P wave with what looks to be a seemingly normal PR interval in lead V4 (ie, of ~0.14 second in duration). QRS morphology for the 3 leads that we see in simultaneously-recorded leads V4,V5,V6 — appears to be typical for LBBB conduction.
• Alternatively (ie, because the PR interval looks to be shorter than 0.14 second in lead V6) — it could be that a sinus P wave and a delayed ventricular escape beat both occurred at about the same time. Clinically — this patient's primary diagnosis remains the same regardless of whether beat #7 is (or is not) conducted.
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• Following beat #7 — there is another extended pause of at least 2 seconds (ie, We see ~10 large boxes without a beat) — at which point the rhythm strip ends.

IMPRESSION:

• Today's patient should be assumed to have SSS (Sick Sinus Syndrome) — until you can prove otherwise.

Figure-2: I've counted the number of large boxes between beat #6 and beat #7. As can be seen — the pause is more than 24 large boxes = nearly 5 seconds in duration! (See text).

A Closer Look at Today's Case:

The ECG in Figure-2 provides an excellent example of how a patient with SSS (= Sick Sinus Syndrome) may present.

• SSS is by far the most common reason for permanent pacemaker placement. The entity becomes increasingly common as the population ages — especially in patients over 60-70 years of age. There is often a long subclinical period (of up to a decade or more!) — during which sinus bradycardia and arrhythmia are seen — but not to a degree that produces symptoms.
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• PEARL #1: Perhaps the easiest way to remember the arrhythmias most commonly associated with SSS — is to think of what one might expect IF the SA node became “sick”. Therefore: i) The most common initial rhythm with SSS will be sinus bradycardia and arrhythmia; ii) Some months (or years) afterwards — increasingly long sinus pauses (which may ultimately lead to sinus arrest) — and various forms of SA nodal block may occur; iii) Typically, there is not just SA nodal disease — but also AV nodal disease and AV block — with resultant slowing of the AV nodal escape rate in response to increasingly long pauses or other forms of bradycardia; iv) Many patients also have a “Tachy-Brady” syndrome — in which tachyarrhythmias (most commonly rapid AFib) alternate with periods of bradycardia; and, v) Because the SA node is “sick” — the SA node recovery time is often prolonged. As a result — long pauses commonly follow episodes of tachycardia (because tachycardia episodes result in SA node suppression).
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• PEARL #2: The indication for pacemaker placement with SSS is “symptomatic bradycardia”. Thus, it is not those episodes of rapid AFib that are seen in patients with "Tachy-Brady" Syndrome that qualify — but rather severe bradycardia that causes symptoms! KEY Point: If the only way to control “tachy” episodes is with medication that then produces symptomatic bradycardia — this qualifies as indication for pacemaker placement.
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• PEARL #3: It is important to appreciate that short pauses (ie, between 1.5-2.0 second) are relatively common during ambulatory Holter monitoring. Many of these short pauses are benign. KEY Point: Pauses clearly become cause for concern once they exceed 2.0 second in duration (especially ≥2.5 second). Clear indication for pacing with SSS is generally accepted to be present once pauses attain ≥3.0 second in duration.

PEARL #4: Given the above “Basics of SSS” — diagnosis of this very common syndrome in the elderly becomes surprisingly EASY:

• Suspect SSS whenever an “older patient” presents with inappropriate bradycardia (ie, marked and persistent heart rate slowing — especially when associated with symptoms such as fatigue or syncope; frequent prolonged sinus pauses; slower-than-expected AFib, etc.).
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• Rule out common potentially "fixable" causes of inappropriate bradycardia. These include rate-slowing medication — recent ischemia/infarction — hypothyroidism — sleep apnea. If none of these potentially “fixable” causes are present — then it is almost certain that the older patient in front of you who is presenting with inappropriate bradycardia has SSS.
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• Is Pacing Indicated? — The decision of whether or not pacemaker implantation is indicated then depends on: i) Severity of the disorder — and its direct correlation with symptoms resulting from inappropriate bradycardia; and, ii) Ruling out any "potentially fixable" cause(s).

CONCLUSION to Today's Case:

Unfortunately — I do not have specific follow-up regarding the patient in today's case. That said — We can strongly suspect that a permanent pacemaker will probably be needed in this older patient with notable symptoms.

• ECG features of SSS that appear in Figure-2 include: i) "Tachy-Brady" Syndrome, with rapid AFib (for the first 6 beats in this tracing); and, ii) Post-tachycardia suppression that results in successive prolonged pauses (nearly 5 seconds in duration — followed 1 beat later by another prolonged pause).
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• KEY Point: As emphasized earlier under PEARL #4 — potentially "fixable" causes of inappropriate bradycardia need to be ruled out before we can establish the diagnosis of SSS. 
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• I suspect that beat #7 in ECG #1 is conducted. If so — then this beat is conducted with LBBB. This would be an example of a paradoxical (ie, bradycardia-induced) conduction defect — and would further suggest the likelihood of underlying heart disease.
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• Realistically — it's hard to imagine that a "fixable cause" will be found that will be able to reverse this degree of SA node suppression (with such excessive pauses). I suspect that close observation during a brief hospitalization will establish definitive need for a pacemaker.
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• P.S. (3/27/2024): Other descriptions might be used for the extended pause of nearly 5 seconds in Figure-2 — including transient ventricular standstill and/or PD-PAVB (Pause-Dependent Paroxysmal AtrioVentricular Block) — although as described in ECG Blog #419, cessation of atrial activity as well as ventricular escape is against "PD-PAVB". That said, regardless of the terminology used — the "Bottom Lines" remain the same: i) This patient almost certainly has advanced SSS; and, ii) Permanent pacing will almost certainly be needed.

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Acknowledgment: My appreciation to Evan MacIntyre (from North Carolina, USA) for the case and this tracing.

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ADDENDUM (November 3, 2022):

• The Audio PEARL (2:45 minutes) below reviews the ECG findings of SSS.

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Related ECG Blog Posts to Today’s Case: 

ECG Blog #185 — Reviews the Ps, Qs and 3R Approach to Systematic Rhythm Interpretation.

ECG Blog #256 — Reviews another case of SSS (Sick Sinus Syndrome).

ECG Blog #295 — Reviews the concept of bradycardic-induced BBB ( = Phase 4 block). This is discussed near the bottom of the page (ie, in Pearl #5 — that appears just under Figure-6).

The July 5, 2018 post in Dr. Smith's ECG Blog — (Please see My Comment at the bottom of the page for Review on the ECG diagnosis of Sick Sinus Syndrome).