ECG Blog #332 — 3rd-Degree with Double BBB?

The ECG in Figure-1 — is from a woman in her 60s, who presented with “chest tightness” over several days. This tracing was diagnosed as showing complete AV block.

QUESTIONS:

• Do YOU agree with the interpretation? OR — Is this “trifascicular" block?
• Is there evidence of infarction on this tracing?

Figure-1: 12-lead ECG and long lead II rhythm strip — obtained from a woman with "chest tightness" over several days. Is this complete AV block? — Is it "trifascicular" block? (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the ECG in Figure-1:

As always – I favor beginning interpretation with assessment of the long lead rhythm strip — using the Ps, Qs & 3R Approach to recall the 5 KEY Parameters (See ECG Blog 185). I find it easiest (and most productive) to delay assessing the 12-lead ECG until after I’ve had a chance to look at the rhythm.

PEARL #1: As I have often emphasized — It does not matter in what sequence you choose to assess the 5 KEY Parameters — and I often START with whichever of these parameters is easiest to assess.

• Today's tracing is extremely complicated. On initial inspection of this rhythm — it simply is not immediately evident: i) Why QRS morphology is changing? (ie, Bundle branch block or ventricular escape beats?); ii) Why the ventricular rate is changing? — and, iii) What kind of AV block is present?
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• As a result of the above complexities — My "eye" focused on beat #4 in Figure-1 because: i) This beat occurs earlier-than-expected; ii) The QRS complex of beat #4 is not as wide as the QRS in the first 3 beats; and, iii) The PR interval preceding beat #4 = 0.18 second, which makes it the only one of the 6 beats on this tracing that is preceded by a PR interval with a reasonable chance of conducting. 

 

PEARL #2: When a complex form of AV block is present — my favorite CLUE that a beat is likely to be conducted — is IF you see a beat that occurs earlier-than-expected.

• In addition to its earlier-than-expected occurrence — further support that beat #4 in Figure-1 is probably conducted is forthcoming from: i) The fact that QRS morphology changes from that of the 3 preceding beats; ii) A look at simultaneously-recorded lead V1 for beat #4 suggests a very typical RBBB (Right Bundle Branch Block) morphology — in the form of an rSR' (with S wave descending below the baseline in lead V1 — and a terminal "taller right rabbit ear" R' deflection); and, iii) Beat #4 is the only beat preceded by a normal PR interval — whereas the none of the other PR intervals preceding the remaining 5 beats on this tracing seem likely to conduct.
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• NOTE: For more on HOW to tell if a P wave is (or is not) likely to conduct — Check Out the Audio Pearl in the ADDENDUM below.

PEARL #3: As I often emphasize — the simple step of labeling P waves is amazingly helpful for: i) Determining IF there is an underlying regular (or almost regular) atrial rhythm; and, ii) Facilitating assessment as to whether some (or all) of the P waves you identify are (or are not) Related to neighboring QRS complexes.

• In Figure-1 — I began my “Search for P Waves” — by labeling those P waves that I was certain are present. I have done this with RED arrows in Figure-2.
• Accounting for slight variation in the P-P interval that is so often seen — it seems logical to anticipate that 2 additional sinus P waves are likely to be hiding within the QRS of beats #1 and 2 (PINK arrows in Figure-2).

PEARL #4: It is common to see slight variation in the atrial rate when there is 2nd- or 3rd-degree AV block. This phenomenon is known as ventriculophasic sinus arrhythmia — and is thought to be due to better perfusion for those P waves that "sandwich" a QRS complex (with resultant slight shortening of the P-P interval). There may then be slight lengthening for P-P intervals that do not contain a QRS between them.

• To Emphasize: The above relationship showing slight shortening of the P-P interval for those P waves that "sandwich" a QRS complex between them — does not always hold. That said — we do for the most part see this relationship hold true for most P-P intervals shown in Figure-2.

QUESTION:

• Doesn't the labeling of P waves with ARROWS in Figure-2 — facilitate determining which of the P waves in today's tracing are likely to have a chance to conduct?

Figure-2: I have added RED arrows over those P waves that I am certain are present in the long lead II rhythm strip.

Is There Complete AV Block in Figure-2?

Ideally — we would have a much longer period of monitoring for determining the rhythm in Figure-2. That said — I find it helpful to break down our assessment of the rhythm into several Parts:

• Part-1: Look at the first 3 beats in Figure-2. The QRS complex for these first 3 beats is wide — with a morphology potentially consistent with LBBB (Left Bundle Branch Block).
• The 6 P waves associated with these first 3 beats appear completely unrelated to the QRS (ie, with a constantly changing PR interval). The 1st, 3rd and 5th P waves in the long lead II rhythm strip ( = the first 3 RED arrows) have clearly had more than adequate opportunity to conduct — yet failed to do so. This suggests that at the least — there is high-grade 2nd-degree AV Block.
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• Part-2: As we have already deduced (ie, in Pearls #1 and #2 above) — the degree of AV block for the rhythm in Figure-2 can not be "complete" — because beat #4 is conducted! We know this — because beat #4 occurs earlier-than-expected — beat #4 is preceded by a normal PR interval — and QRS morphology of this beat #4 changes from the LBBB-like appearance of the first 3 beats in Figure-2 — to a QRS morphology consistent with RBBB conduction.
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• Part-3: The remaining 2 beats in Figure-2 ( = beats #5 and 6) are not conducted. We know this because: i) None of the P waves associated with these last 2 QRS complexes occur at a point in the cardiac cycle when they would be expected to conduct; and, ii) The R-R intervals between beats #4-5 and beats #5-6 are equal to each other — and — these R-R intervals are significantly longer than the R-R interval preceding beat #4 that we know is conducting. This suggests that beats #5 and 6 must be "escape" beats that manifest (at least in lead II) a similar QRS morphology as conducted beat #4.

Figure-2: Putting It All Together 

• High-grade 2nd-degree AV Block is present in the long lead II rhythm strip in Figure-2 — because there are many P waves that clearly have more than adequate opportunity to conduct, yet fail to do so. But because at least 1 QRS complex is conducted (ie, beat #4) — the degree of AV block can not be complete!
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• The 1 beat in Figure-2 that is conducted ( = beat #4) — is conducted with an underlying RBBB (based on the typical rSR' morphology of this beat in lead V1 — as was highlighted in Pearl #2 above).
• Because QRS morphology of "escape" beats #5 and 6 in the long lead II rhythm strip is similar to QRS morphology of conducted beat #4 — this suggests that the site of these escape beats is from the AV Node. The wide terminal S wave in simultaneously-recorded lateral leads V5 and V6 for beat #6 — is consistent with RBBB conduction.
• Presumably — the first 3 beats in this tracing, that manifest AV dissociation with more pronounced QRS widening (ie, beats #1,2,3) — are arising from an "escape" site below the AV Node (ie, either from the right bundle branch or from ventricular myocardium).

QUESTION:

• What do the measurements that I've added in Figure-3 show?

Figure-3: I've measured the R-R intervals between each of the beats in today's rhythm. I've also dropped 3 vertical BLUE lines to show where the QRS complex begins for beats #1, 4 and 6 in simultaneously-recorded leads.

Figure-3: What Do My Measurements Show?

When I first saw today's tracing — I wondered if beats #1,2,3 might be supraventricular, given the close resemblance of QRS morphology for these beats to LBBB conduction. As a result — I initially wondered if alternating BBB (Bundle Branch Block) might be present — with change from LBBB to RBBB conduction beginning with beat #4?

• I found it interesting that caliper measurement reveals an equal R-R interval between beats #1-2 and beats #2-3 ( = 1480 msec.) — and — that this R-R interval is different than the R-R interval between beats #4-5 and beats #5-6 ( = 1530 msec.). The fact that these 2 R-R intervals are different — suggests there are 2 different "escape" rhythm sites.
• The finding of similar (if not identical) QRS morphology for conducted beat #4 — and non-conducted "escape" beats #5,6 — essentially localizes the site of this "escape" focus to the AV Node.
• I thought this finding made it much more likely that beats #1,2,3 represent a ventricular escape focus (possibly arising from the right bundle branch).
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• Finally — I dropped verticle BLUE lines passing through simultaneously-recorded leads for beats #1, 4 and 6. These lines begin just before the onset of the QRS complex. They explain why despite RBBB conduction — the QRS complex does not look overly wide for beats #4,5,6 in the long lead II rhythm strip (ie, the initial part of the QRS in lead II lies isoelectric with the baseline).

Is There Evidence of Infarction in Figure-3?

Common things are common. Given the presence of bradycardia + high-grade 2nd-degree AV block + underlying RBBB — recent infarction has to be strongly considered as the potential precipitating factor for these multiple conduction defects.

• Assessment of ST-T wave changes during a ventricular rhythm is usually difficult (and often not possible). As a result — I did not think much could be said about the possibility of recent infarction from assessment of ST-T wave appearance of beats #1,2,3 in Figure-3 — because these first 3 beats in the rhythm presumably arise from a ventricular escape focus.
• Beats #4,5,6 manifest RBBB conduction. While not definitive — I thought the appearance of ST-T waves in several of the chest leads leads in which this supraventricular RBBB conduction morphology appears was potentially suspicious for a recent (or acute) cardiac event. That is: i) Usually the ST segment in lead V1 with RBBB is depressed — and not at the baseline, as it is in Figure-3. There is also usually no terminal T wave positivity with RBBB in lead V1; ii) ST depression with RBBB is usually also seen in lead V2 — so the distinctly flat ST segment that we see in lead V2 of Figure-3 is not typical; and, iii) The T waves in leads V5,V6 appear larger-than-expected given R wave amplitude in these leads (ie, These T waves may be hyperacute).
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• To Emphasize: The above described ST-T wave changes are not definitive. Instead — they are subtle! But in the setting of the advanced conduction defects that we see in today’s tracing — these subtle ST-T wave changes are suspicious for a possible recent event — and — this suspicion justifies obtaining serial tracings and troponins, and possibly performing cardiac catheterization (depending on specifics of the clinical situation).

Is There Tri-Fascicular Block?

The term, “trifascicular” block — implies impaired conduction in all 3 of the major conduction fascicles: i) the right bundle branch; ii) the left anterior hemifascicle; and, iii) the left posterior hemifascicle.

• The term, “trifascicular block” is no longer recommended (Surawicz et al — JACC: Vol. 53, No. 11, pp 976-981, 2009). This is because of “the great variation in anatomy and pathology producing this pattern” — as well as the fact that one will usually not be able to make a definitive diagnosis of trifascicular block from the surface ECG. We simply can not tell IF PR interval prolongation in a patient with bifascicular block is due to AV Nodal disease or disease in the remaining conducting fascicle.
• The Exception: Rarely, one may be able to diagnose involvement in all 3 conduction fascicles — if for example, there is RBBB and LAHB that alternates with RBBB/LPHB. But even in this circumstance — current recommendations favor clarity in description by avoiding the term “trifascicular block” — and instead noting each of the conduction defects that are present.
• Regarding Today’s Tracing: As stated above — the conduction defects in today’s tracing include: i) High-grade 2nd-degree AV block (but not complete AV block!); and, ii) Underlying RBBB for the 1 conducted beat, and for the 2 AV Nodal escape beats. Since there is no indication of either left anterior or posterior hemiblock — there is no evidence in today's tracing for “trifascicular” block.

Final Confirmation of the Rhythm in Today's Case:

The BEST way to demonstrate the etiology of a complex cardiac rhythm — is by construction of a Laddergram — which I illustrate in Figure-4.

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• NOTE: For more on how to read (and/or draw) Laddergrams — Please check out our ECG Blog #188 (which includes teaching aids + LINKS to more than 50 illustrated laddergrams I have published).   

Figure-4: My proposed laddergram for explaining the mechanism of today’s rhythm (See below).

Explanation of the Laddergram in Figure-4:

• The first 3 beats in the long lead II rhythm strip most likely represent a ventricular escape rhythm (which is why these beats originate from the bottom of the Ventricular Tier). None of the first 6 P waves (labeled "a"-thru-"f") are able to conduct to the ventricles — so there is AV dissociation during the first half of this tracing.
• The KEY to interpreting today’s rhythm lies with recognition that beat #4 is conducted, albeit with RBBB. The fact that at least 1 on-time P wave (this being the P wave labeled “g”) is able to conduct — tells us that the degree of AV block is not complete.
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• Following beat #4 — there is again AV dissociation, as none of the next 5 on-time P waves (labeled "h"-thru-"l") are conducted to the ventricles.
• While true that the on-time P waves labeled “i” and “k” do not have a reasonable “chance” to conduct (because they either occur with a PR interval that is too short to conduct — or they occur right after the QRS during the absolute refractory period) — the P waves labeled “h”, and especially “j” should be able to conduct, but fail to do so. This supports our conclusion that there is high-grade 2nd-degree AV block.
• Since the R-R intervals between beats #4-5 and beats #5-6 are equal to each other, and clearly longer than the R-R interval preceding conducted beat #4 — and — since QRS morphology of beats #5 and 6 is similar (if not identical) to QRS morphology of conducted beat #4 — beats #5 and 6 presumably represent a junctional escape focus that also manifests RBBB conduction.

CASE Follow-Up:

Unfortunately, my follow-up to today’s case is limited. I know that troponin was normal — and that the patient did not have hyperkalemia. A permanent pacemaker was placed — and the patient was discharged from the hospital after several days without further complication.

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Acknowledgment: My appreciation to 林柏志 (from Taiwan) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation. (This block post also reviews the concept of "Trifascicular Block").
• ECG Blog #185 — Use of a Systematic Approach to Rhythm Interpretation. 
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• ECG Blog #188 — Reviews how to read (and/or draw) Laddergrams (plus LINKS to more than 50 clinical examples of laddergrams I have drawn).
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• ECG Blog #203 — Reviews the ECG diagnosis of Axis and Hemiblocks.
• ECG Blog #204 — Reviews a user-friendly approach for diagnosis of the Bundle Branch Blocks.
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• ECG Blog #186 — and ECG Blog #236 — for review on the basics of 2nd-degree AV Block.
• ECG Blog #192 — Reviews the 3 Causes of AV Dissociation — and emphasizes why AV Dissociation is not the same thing as Complete AV Block. 

• ECG Blog #191 — Emphasizes the difference between AV Dissociation vs Complete AV Block.
• ECG Blog #202 — and ECG Blog #257 — Review cases regarding HOW to tell if there is (or is not) Complete AV Block.
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• ECG Blog #247 — Reviews a complex case with AV Dissociation.

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ADDENDUM (9/14/2022): I've reviewed some KEY material related to today's case:

• Audio Pearl on HOW to tell if a given P wave in an AV block tracing is likely to be conducting.
• 3 figures below (from my ECG-2014-PB) — that review "My Take" on the ECG diagnosis of Bifascicular Block.

—  — 

ECG Media PEARL #61 (5:45 minutes Audio) — Reviews HOW to Tell IF a P Wave is Conducting? Being able to answer this question is KEY for determining the etiology of complicated AV Block/AV Dissociation tracings.

Figure-5: RBBB/LAHB — RBBB/LPHB.

 

Figure-6: RBBB/LPHB (cont.) — ECG examples of bifascicular block.

 

Figure-7: Trifascicular Block? — Isolated LPHB vs marked RAD.

ECG Blog #331 — What's The Rhythm?

I was sent the ECG in Figure-1 — but without the benefit of clinical information. There apparently were a number of different opinions by clinicians regarding interpretation of this rhythm.

• How would YOU interpret the ECG in Figure-1?
• Is there complete AV block?

Figure-1: The 12-lead ECG and simultaneously-recorded long lead II rhythm strip in today’s case.

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NOTE: Interpretation of today's rhythm is challenging for a number of reasons. As a result — I go step-by-step in walking through my approach to this tracing.

• IF you prefer to skip the "step-by-step" (and go directly to the answer) — Scroll down to Figure-11 at the bottom of this page (to find the last laddergram with the Final Answer!). 

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MY Thoughts on the ECG in Figure-1:

As always – I favor beginning interpretation with assessment of the long lead rhythm strip — using the Ps, Qs & 3R Approach to recall the 5 KEY Parameters (See ECG Blog 185). I find it easiest (and most productive) to delay assessing the 12-lead ECG until after I’ve had a chance to look at the rhythm.

PEARL #1: It does not matter in what sequence you choose to assess the 5 KEY Parameters — and I often start with whichever of these parameters is easiest to assess. For example — although I do see a number of P waves in the long lead II rhythm strip in Figure-1 — I found it easier to begin by looking at QRS width and Regularity of the rhythm. I approached this tracing as follows:

• QRS Width: Looking at all 12 leads (to see where the QRS interval is longest) — it should be apparent that the QRS complex is narrow (ie, not more than 0.10 second = not more than half a large box in duration in any lead). Knowing that all QRS complexes in today’s tracing are narrow — tells us that the rhyhthm is supraventricular.
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• Regularity of the Rhythm: It should be obvious that the rhythm in the long lead II rhythm strip is not Regular. Instead — each R-R interval appears to be slightly different than its neighboring R-R interval — so the rhythm is irregular.
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• Rate of the Rhythm: R-R intervals in the long lead II rhythm strip vary from just over 4 large boxes in duration — to a bit over 6 large boxes in duration — which suggests an average heart Rate of ~60/minute.
• Alternatively — You could arrivate at a similar estimated heart rate considering that there are 10 beats in this 10-second rhythm strip.

Continuing with my Ps, Qs, 3R Assessment:

The above process left me still having to assess the 2 remaining Parameters ( = P waves — and — Whether any P waves that are present are Related to neighoring QRS complexes?):

• P Waves: A number of P waves are definitely present!

PEARL #2: As emphasized in previous ECG Blogs — I have found the simple step of labeling P waves to be surprisingly helpful for: i) Determining IF there is an underlying regular (or almost regular) atrial rhythm; and, ii) Facilitating assessment as to whether some (or all) of the P waves you identify are (or are not) Related to neighboring QRS complexes.

• I favor beginning my “Search for P Waves” — by labeling those P waves that I am certain are present. I have done this with RED arrows in Figure-2.

Figure-2: I have added RED arrows over those P waves that I am certain are present in the long lead II rhythm strip.

MY Thoughts on Figure-2:

I see at least 9 definite P waves in Figure-2 (RED arrows). For these 9 P waves — the duration of the P-P interval between neighboring P waves looks similar (albeit not quite identical).

PEARL #3: Often when I am able to identify a number of definite P waves in a complex rhythm (as I've done for the RED arrows in Figure-2) — in which the duration of P-P intervals between neighboring P waves is similar (as it is in Figure-2) — additional "on-time" P waves can be found within the QRS complex or ST-T wave of intervening beats.

• Search for such additional “hidden” (or partially hidden) P waves — is facilitated by use of calipers! Simply set your calipers to the P-P interval you measure between 2 of the RED arrows — and see IF there is evidence of notching (or other subtle alteration in one or more T wave deflections) at this caliper-set distance within those R-R intervals that seem to be missing a RED arrow (ie, within the R-R intervals between beats #1-2 — between beats #4-5 — between beats #5-6 — and between beats #9-10).
• I have done this by adding YELLOW arrows to Figure-2 in these places (See Figure-3). It should be apparent that the reason the T waves of beats #1, 4, 5 and 9 all look slightly different from one another in Figure-3 —  is that an “on-time” P wave is partially hidden (and deforming) the T wave for each of these beats.

Figure-3: I've added YELLOW arrows to Figure-2 in places where an "on-time" P wave appears to be hiding (and partially deforming) the T waves of beats #1,4,5 and 9.

An Underlying Sinus Rhythm Is Present!

We have therefore established in Figure-3 — that an underlying sinus rhythm is present in today's rhythm. For clarity — I've highlighted each of the upright sinus P waves in Figure-4 with a RED arrow in the long lead II rhythm strip.

• IF up until now, you have used calipers to assist in location of the partially hidden P waves — you will have noticed slight variation in duration of the P-P intervals in Figure-4. This is because a component of sinus arrhythmia is present.
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• Did YOU Notice that there are 13 P waves (RED arrows) — but only 10 QRS complexes in Figure-4? This is because not all P waves are conducted. The fact that there are more P waves than QRS complexes in Figure-4 — suggests that some form of 2nd-degree AV block is likely to be present.

QUESTION:

• Do YOU think that any of the P waves in Figure-4 are being conducted to the ventricles? (HINT: Are the PR intervals before any of the 10 beats on this tracing the same?).   

Figure-4: RED arrows highlight a fairly regular sinus rhythm — which manifests slight variation in the P-P interval (sinus arrhythmia). Do YOU think any of the sinus P waves in this tracing are conducting? IF so — Which ones?

Are Any P Waves in Figure-4 Conducting?

For clarity in Figure-5 — I've color-coded the ARROWS highlighting sinus P waves in today's rhythm. There are some identical PR intervals on this tracing. 

• The PR intervals preceding beats #2, 7 and 10 are normal (ie, 0.18 second) — and of equal duration to each other (RED arrows in Figure-5). Note that the R-R intervals preceding each of these 3 beats — are the longest R-R intervals in this tracing.
• PEARL #4: The fact that there are a number of identical PR intervals in today's tracing is unlikely to be due to chance — and tells us that these P waves are being conducted to the ventricles. The presence of conducted beats rules out complete AV block!
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• The PR intervals preceding beats #3 and 8 are of similar (but not identical) duration. I color-coded these 2 P waves with different shades of BLUE to indicate that while this PR interval before beats #3 and 8 is clearly longer than the PR interval highlighted by the RED arrows — there is a slight difference in PR interval duration (ie, the PR interval before beat #8 is slightly longer than the PR interval before beat #3).
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• The PR intervals before beats #4 and 9 are equal and longer still (ie, 0.50 second — highlighted by GREEN arrows in Figure-5)!

PEARL #5: Considering our previous suspicion that some form of 2nd-degree AV block is present (because of the finding that more P waves than QRS complexes are present) — and — the finding of identical PR intervals at the end of each relative pause (ie, before beats #2,7,10 — RED arrows) — and — the finding of progressive PR interval lengthening within groups (ie, from RED-to BLUE-to GREEN arrows) — Doesn't This Suggest that the type of 2nd-degree AV block that is present is most likely to be some form of Mobitz I ( = AV Wenckebach)?

• WHITE arrows near the beginning of each of the longer R-R intervals — appear to represent non-conducted P waves (that are partially hidden within the T waves of beats #1, 6 and 9). It should not be unexpected that these P waves are non-conducted — because they occur so early in the cycle (ie, at a time when the ventricles will probably be refractory).
• This leaves us with only 3 more P waves to account for (ie, the BLACK arrows in Figure-5). Wouldn't It Make Sense for the BLACK arrows after beats #4 and 5 to be conducting with progressively longer PR intervals — until finally, the WHITE arrow P wave after beat #6 is blocked — before the next Wenckebach cycle begins with a much shorter (and normal) PR interval before beat #7 (RED arrow)?

Figure-5: I've color-coded the sinus P waves in Figure-4 — to facilitate recognizing beats with similar PR intervals.

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To EMPHASIZE: Although I have described the above series of rhythm-solving steps in great detail — use of calipers — and awareness of what to look for — allowed me to solve this complex arrhythmia within 2-to-3 minutes! This process can be done quickly!

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PEARL #6: I suspect that virtually all readers of my ECG Blog are familiar with the basic pattern of the Mobitz I form of 2nd-degree AV Block ( = AV Wenckebach). In "typical" Mobitz I — there is a regular atrial rhythm — and, the PR interval progressively lengthens until a beat is dropped. There follows a short pause — and then the next Wenckebach cycle begins again.

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• WHY was today's rhythm so challenging to interpret?

ANSWER:

There are numerous variations on the theme of Wenckebach blocks (See ECG Blog #251 for discussion — with an Audio Pearl on the "Footprints" of Wenckebach). PEARL #6 (above) — is to appreciate how today's rhythm represents a more subtle variation on the "usual" Wenckebach theme. Reasons why this rhythm may not have been recognized by the clinicians who initially saw the patient include:

• The pauses containing the dropped beats are not much longer than many of the other R-R intervals in this tracing. At first glance — today's rhythm looks to be almost regular.
• The 2 "groups" of beats in today's tracings (ie, beats #2-thru-6; and #7-9) do not "look" similar (whereas many Mobitz I tracings feature similar 2-beat or 3-beat groupings).
• With typical Mobitz I tracings — the greatest "increment" in PR interval (ie, the amount that the PR interval increases from one beat-to-the-next) — occurs between the 1st and 2nd beats within a group. This is not what we see in today's tracing — as the greatest increment in PR interval is seen when moving from BLUE arrow to GREEN arrow P waves.
• Finally — The BLACK arrow P waves before beats #5 and 6 are conducted with unusually long PR intervals (ie, 0.64 and 0.68 second, respectively). As a result — it may not seem likely that these BLACK arrow P waves can be conducting.

Final Thoughts on Today's ECG:

The rhythm in today's case represents an unusual example of 2nd-degree AV Block of the Mobitz I Type ( = AV Wenckebach). Whether the unexpected increase in PR interval between the 2nd and 3rd beat in each grouping is the result of dual AV Nodal pathways — or simply "variation-on-the-theme" is uncertain — and probably not important for this patient's clinical course. The "good news" — is that the overall ventricular response is not slow — so it is possible that this patient may not be symptomatic. Unfortunately — We were not provided with any clinical history.

• After interpreting the rhythm in today's case — we need to assess the remainder of the 12-lead ECG. Although we do not know the age of this patient — QRS amplitude appears to be markedly increased (ie, very deep S wave >25 mm in lead V2 — and tall R waves in the lateral chest leads) — so LVH is suspected.
• The negative T wave in lead III is not necessarily abnormal given predominant negativity of the QRS in this lead. There do not appear to be any acute ST-T wave changes.
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• Clinical Correlation will be essential for optimal management in today's case! In ECG Blog #307 — we explored the most important clinical conditions associated with 2nd-degree or 3rd-degree AV block (See Figure-6 in ECG Blog #307). Although acute inferior infarction is probably the most common cause of AV Wenckebach — there is no indication of this on today's ECG. There is however probable LVH — so full evaluation of this patient for an underlying cardiac cause of this AV conduction disturbance is in order.

Final Confirmation of the Rhythm in Today's Case:

The BEST way to demonstrate the etiology of a complex cardiac rhythm — is by sequential construction of a Laddergram — which we illustrate in step-by-step fashion through the next 6 Figures.

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• NOTE: For more on how to read (and/or draw) Laddergrams — Please check out our ECG Blog #188 (which includes teaching aids + LINKS to more than 50 illustrated laddergrams I have published).   

Beginning with Figure-6:

Figure-6: It's easiest to begin construction of a laddergram by indicating atrial activity. Vertical RED lines in the Atrial Tier correspond to P waves (RED arrows) in the long lead II rhythm strip.

Figure-7: Next — I've filled in the Ventricular Tier with RED arrows that correspond to each of the QRS complexes in the long lead II. Note that it will often be easy to fill in the Atrial and Ventricular Tiers (as I've done in Figures-6 and -7). The "challenge" for solving the arrhythmia — usually begins with filling in the AV Nodal Tier (This comes next!).

Figure-8: It's time to start filling in the AV Nodal Tier. It's easiest to begin with those beats that you know are conducting ( = beats #2, 7 and 10 — each of which are preceded by the same normal PR interval).

Figure-9: I next focused on the 1st group of beats (ie, beats #2-thru-6). It seemed logical that the BLUE arrow P wave would be conducting beat #3 (with a slight increase in PR interval compared to the PR interval of beat #2) — to be followed by the GREEN arrow P wave conducting beat #4. Looking "ahead" — this leaves us with the remaining 3 RED arrow P waves in this 1st group — but with only 2 QRS complexes ( = beats #5,6).

Figure-10: I've connected the RED arrow P waves that occur within the T waves of beats #4 and 5 — to the only logical QRS complexes that might be conducted by them. This means that the RED arrow P wave that occurs just after the QRS of beat #6 must be non-conducted!

Figure-11: I then completed my proposed laddergram by connecting the remaining RED arrow P waves to the only logical QRS complexes that might be conducted by them. As deduced earlier — it is logical that the WHITE arrow P waves are not conducted — because they occur so early in the cycle (very soon after the previous QRS complex).

CONCLUSION: It should be apparent from this laddergram that there are 2 Wenckebach groupings — in which PR intervals progressively increase from beats #2-thru-6 (until the WHITE arrow P wave occurring just after beat #6 is blocked) — and a shorter Wenckebach grouping (beats #7-9), with increasing PR interval until the WHITE arrow P wave after beat #9 is blocked. Thus, the rhythm in today's case = 2nd-degree AV Block, Mobitz Type I (AV Wenckebach) with 6:5 and 4:3 AV conduction.

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Acknowledgment: My appreciation to Arkan KaDhim (from Baghdad, Iraq) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation. 
• ECG Blog #185 — Reviews my Systematic Approach to Rhythm Interpretation.
• 
  
• ECG Blog #188 — Reviews how to read (and/or draw) Laddergrams (plus LINKS to more than 50 clinical examples of laddergrams I have drawn).
• 
  
• ECG Blog #186 — and ECG Blog #236 — for review on the basics of 2nd-degree AV Block.
• 
  
• ECG Blog #192 — Reviews the 3 Causes of AV Dissociation — and emphasizes why AV Dissociation is not the same thing as Complete AV Block. 
• ECG Blog #191 — Emphasizes the difference between AV Dissociation vs Complete AV Block.

ECG Blog #330 - Pneumonia with 2 ECG Findings!

Today’s patient is an elderly man who was admitted to the hospital for symptoms of fever and coughing — with an admission diagnosis of community-acquired pneumonia. He was treated with antibiotics. A short while after hospital admission — the patient complained of chest pain, at which time the ECG in Figure-1 was obtained. 

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

Figure-1: This ECG was obtained for an episode of chest pain. The patient is an elderly man admitted to the hospital for pneumonia.

MY Thoughts on the ECG in Figure-1: 

Unfortunately — there is no long lead rhythm strip for ECG #1. In addition — resolution is suboptimal, and the wide black lead change markers may be concealing beats. I suspect the rhythm is supraventricular with PACs (Premature Atrial Contractions) — but a longer rhythm strip lead would be needed to verify this.

• PEARL #1: Something is wrong! You virtually never normally see an almost-all-negative QRS complex in lead I (especially when the T wave is also negative in this lead).
• Further increasing my suspicion that something is wrong with this initial ECG in Figure-1 — is the finding of an all-positive QRS with positive T wave in lead aVR.
• 
  
• PEARL #2: Doesn't the QRS complex and ST-T wave in lead I — look like what we'd expect the QRS and ST-T wave to normally look like in lead aVR? (And doesn't the QRST in lead aVR — look like what we'd expect the QRST in lead I to look like?). This reversal from our normal expectations for the QRST in leads I and aVR strongly suggests there is LA-RA (ie, Left Arm-Right Arm) Lead Reversal.
• 
  
• PEARL #3: We can usually quickly distinguish between LA-RA lead reversal vs dextrocardia — by looking at R wave progression in the chest leads. Because the heart lies in the right hemithorax when there is dextrocardia — you will usually see "reverse" R wave progression in the chest leads (ie, R wave ampitude becoming progressively smaller as one moves across the chest from lead V1-to-V6).
• LA-RA lead reversal is much more common than dextrocardia. In Figure-1 — R wave amplitude is increasing as one moves from lead V1-toV6, so I thought it unlikely that dextrocardia was present. That said — given how small R wave amplitude still is in the most lateral chest lead ( = lead V6) — I was not yet 100% certain that dextrocardia was ruled out.

BOTTOM LINE: The ECG in Figure-1 — should be promptly repeated! There are at least 2 reasons for this:

• Reason #1: We want to see what this patient's ECG looks like with electrode leads correctly placed. (Along the way — we'll listen to the patient chest to verify that heart sounds are on the left and not the right side of the thorax).
• Reason #2: There are a number of abnormal findings in the inferior leads in the ECG shown in Figure-1 — including Q waves, ST elevation and T wave inversion. Is this patient having an acute inferior MI?

The CASE Continues:

The lead reversal was not recognized — so the ECG in Figure-1 was never repeated.

• Fortunately — there was another ECG available from this patient for comparison. As stated above — ECG #1 was obtained a short while after hospital admission, when this patient (who had been admitted for pneumonia) — developed chest pain.
• For clarity — I have put the 2 ECGs that were obtained on today's patient together in Figure-2. I've labeled the hospital admission tracing as ECG #2 — which was done as part of the routine procedure for a patient admitted with pneumonia. To Emphasize: The patient was not having any chest pain at the time ECG #2 was recorded.

QUESTION:

• Does your comparison of the 2 ECGs in Figure-2 confirm your interpretation of ECG #1?

Figure-2: The 2 ECGs that were obtained on today's patient.

How Figure-2 Helps:

Seeing what the hospital admission ECG looked like (as we do in Figure-2) — confirms that there was LA-RA Lead Reversal in ECG #1.

• Note that leads I and aVR in the admission ECG ( = ECG #2) look as we expect them to — with an upright QRS complex and upright T wave in lead I — and — a predominantly negative QRS and no upright T wave in lead aVR.
• There is no doubt that R wave progression is normal in ECG #2 (with transition where the R wave becomes taller than the S wave is deep, occurring as expected between leads V3-to-V4).

What Happens with LA-RA Lead Reversal?

My favorite on-line “Quick GO-TO” reference for the most common types of lead misplacement comes from LITFL ( = Life-In-The-Fast-Lane). I have used the superb web page they post in their web site on this subject for years. It’s EASY to find — Simply put in, “LITFL Lead Reversal” in the Search bar — and the link comes up instantly.

• This LITFL web page describes the 7 most common lead reversals. There are other possibilities (ie, in which there may be misplacement of multiple leads) — but these are less common and more difficult to predict.
• By far (!) — the most common Lead Reversal is mix-up of the LA (Left Arm) and RA (Right Arm) electrodes. This is the mix-up that occurred in today’s case. For clarity — I’ve reproduced the illustration from LITFL on LA-RA reversal in Figure-3.

Figure-3: LA-RA Lead Reversal (adapted from LITFL).

What Should ECG #1 Look Like?

For clarity — I've taken the initial ECG in today's case ( = ECG #1) — and inverted lead I — switched leads II and III — and switched leads aVL and aVR ( = ECG #1A, which is the lower tracing in Figure-4).

• Doesn't ECG #1A now look perfectly consistent with what we would expect ECG #1 to look like? Note that there is now: i) A positive R wave and positive T wave in leads I and aVL; and, ii) An essentially all negative deflection in lead aVR.

Figure-4: Applying the manipulations specified in Figure-3 for LA-RA Lead Reversal — reveals in ECG #1A what the initial ECG in today's case should have looked like IF the LA and RA electrodes had been properly placed.

QUESTION:

• Considering that ECG #1A in Figure-4 shows us what ECG #1 (that was recorded in association with an episode of severe chest pain) should look like — HOW would you interpret ECG #1A?

ANSWER:

For clarity in Figure-5 — I've put the tracing done at the time of hospital admission ( = ECG #2) — together with the "corrected" initial ECG in today's case ( = ECG #1A), that was recorded after hospital admission, when the patient began to have chest pain.

Regarding ECG #2:

• There appears to be a regular supraventricular rhythm at 80-85/minute. It's difficult to tell if this is a sinus or ectopic atrial rhythm because of the baseline artifact (and the lack of a clearly upright P wave in all 3 of the beats shown in lead II).
• The QRS is narrow in ECG #2. LAHB is present (ie, the QRS is very negative in lead aVF — and still predominantly negative in lead II). There is no chamber enlargement.
• A QS complex is seen in lead V1 — but otherwise there are no Q waves. R wave progression is normal — with transition occurring between leads V3-to-V4. S waves persist through to lead V6. ST-T waves show nonspecific flattening of the ST segment (with a hint of ST depression is several leads) — but these changes do not appear to be acute.
• 
  
• IMPRESSION: Since the patient in today's case was admitted for pneumonia, and was not having any chest pain at the time ECG #2 was recorded — it was appropriate to interpret this hospital admission ECG as not suggestive of an acute cardiac process.

Figure-5: Comparison of the "corrected" initial ECG in today's case ( = ECG #1A) — with the hospital admission ECG that was recorded before the onset of chest pain (See text).

Regarding ECG #1A:

• There once again is a fairly regular supraventricular rhythm at ~75/minute, with 2 PACs. Lack of a clearly upright P wave for the 2 beats that we see in lead II suggest that this may not be a sinus rhythm.
• There has been an axis shift since the admission ECG — since the QRS complex in lead II of ECG #1A is no longer predominantly negative.
• 
  
• Each of the inferior leads in ECG #1A show — a Q wave (which is quite large in leads III and aVF) — ST segment coving with a small-but-definite amount of ST elevation — and — T wave inversion. 
• 
  
• There are reciprocal changes in high-lateral leads I and aVL — in the form of ST segment straightening, slight depression, and terminal T wave positivity
• 
  
• I suspect that electrode leads V1 and V2 may have been placed too high on the chest — because both leads show a terminal r'. R wave progression is poor (ie, Transition never occurs in the chest leads). That said — ST-T wave changes in the chest leads do not appear to be acute.

IMPRESSION — Putting It All Together:

The tracing labeled ECG #1A (which shows what ECG #1 would have looked like IF electrode leads had been properly placed) — was obtained in response to new-onset chest pain that only developed after this patient was admitted to the hospital. 

• Comparison of ECG #1A with ECG #2 (in Figure-5) — confirms that the above-described ECG changes are new. In this context — these 2 serial tracings in Figure-5 should be interpreted as indicative of acute inferior OMI (Occlusion-based MI) — until you can prove otherwise. 
• 
  
• Unfortunately — We do not have the details regarding when these 2 ECGs were obtained with respect to the precise timing of when the patient's chest pain began and ended. Without this precise timing — it's impossible to hone in on the sequence of events. For example — The fact that the inferior lead Q waves in ECG #1A are so large (in association with no more than modest ST elevation and T wave inversion) — suggests that some period of time (? hours) — may have passed since the onset of infarction.
• T wave inversion in the inferior leads of ECG #1A — suggests that spontaneous reperfusion may have occurred. IF this patient's chest pain had resolved at the time this ECG was obtained — this would suggest that the "culprit" vessel ( = most likely the RCA = Right Coronary Artery) had spontaneously reperfused, and was now still open.
• 
  
• Finally — Given my suspicion of too-high placement of the V1,V2 electrodes — assessment for possible posterior involvement is problematic.

The "Lessons" To Be Learned:

Unfortunately — the LA-RA Lead Reversal in today's case was not recognized. Neither were the above-described ECG signs suggestive of infarction. Therefore, among the "Lessons to be Learned" from today's case include the following:

• Lead I — usually manifests a predominantly positive QRS complex, because this left-sided lead normally sees the heart’s electrical activity as traveling toward lead I. It is of course possible to have right axis deviation — but you will virtually never see an all-negative (ie, QS) complex in lead I (as we almost did for the Qr complex in ECG #1) — unless there is: i) lead reversal; or ii) dextrocardia.
•  
• Lead aVR — usually manifests a predominantly negative QRS complex, because this right-sided lead normally views the heart’s electrical activity as traveling away from the remote (looking down from the right shoulder) viewpoint of lead aVR. Clearly, there are instances in which the QRS manifests positive activity in lead aVR — but the finding of an all negative QRS in lead I with an all positive QRS in lead aVR is virtually diagnostic of either lead reversal or dextrocardia!
• 
  
• The most time-efficient (and accurate) way to compare serial ECGs — is to interpret one of the ECGs completely — and to then look at both ECGs together — going lead-by-lead between the 2 tracings to see if there are significant differences. Had this been done in today's case — clinicians would have immediately realized that the switch from the predominantly negative Qr pattern in lead I and all positive R wave in lead aVR of ECG #1 — to the almost completely opposite QRS orientation in ECG #2 for these same leads — simply did not make physiologic sense.
• 
  
• Finally — Correlation between the timing of serial ECGs with respect to the presence and relative severity of chest pain at the time each ECG is done — is essential for optimal understanding of the sequence of physiologic events. This is the way to tell IF the "culprit" artery for an acute event is likely to still be occluded — or whether it is more likely to have spontaneously reopened. Awareness of this information is essential for optimal clinical decision-making regarding treatment modalities.

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Acknowledgment: My appreciation to Anis Ahmad and Kianseng Ng (from Malaysia) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
• 
  
• ECG Blog #193 — illustrates use of the Mirror Test to facilitate recognition of acute Posterior MI. This blog post revieews the basics for predicting the "culprit artery". NOTE: The Audio Pearl reviews the concept of why the term "OMI" ( = Occlusion-based MI) should replace the more familiar term STEMI.
•  
• ECG Blog #184 — illustrates the "magical" mirror-image opposite relationship with acute ischemia between lead III and lead aVL (featured in Audio Pearl #2 in this blog post). 
• ECG Blog #222 — Reviews the concept of Dynamic ST-T wave Changes (and how this ECG finding can assist in determining if acute cardiac cath is indicated). 
• ECG Blog #230 — Reviews HOW to compare Serial ECGs (ie, "Are you comparing Apples with Apples or Oranges?"). 
• 
  
• ECG Blog #80 — reviews prediction of the "culprit" artery (and provides another case illustrating the Mirror Test for diagnosis of acute Posterior MI).
•  
• ECG Blog #175 — shows a case of true Dextrocardia! (and reviews the basics about the many different forms of Dextrocardia!).
• ECG Blog #264 — shows a case of LA-RA lead reversal.
• 
  
• The November 19, 2020 post in Dr. Smith's ECG Blog — in which I present an easy-to-overlook but important case in which LA-LL lead reversal was missed (with the "tip-off" being recognition of a taller P wave in lead I > lead II).
• The August 28, 2020 post in Dr. Smith's ECG Blog — My Comment (in my Addendum, at the very bottom of the page) reviews expected findings when there is LA-LL lead reversal (Tipoff = the P in lead I is larger than the P in lead II).
• 
  
• The July 29, 2018 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) reviews this case in which there were 2 technical errors that multiple physicians failed to recognize ( = LA-RA lead reversal and too high placement of leads V1, V2 on the chest). 
• The February 11, 2020 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) reviews this case in which there was LA-RA lead reversal.

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ADDENDUM (9/4/2022):

—  —

ECG Media PEARL #72 (5:45 minutes Audio) — Reviews how to suspect Limb Lead Reversal (especially LA-RA lead reversal).