ECG Blog #412 — Is Cardiac Cath Indicated?

The ECG in Figure-1 was obtained from a middle-aged man with known hypertension — who presented to the ED (Emergency Department) for CP (Chest Pain) over the preceding 2-3 days.

QUESTIONS:

• How would YOU interpret the ECG in Figure-1?
• Should you activate the cath lab?  If not — What next? 

Figure-1: The initial ECG in today's case — obtained from a middle-aged man with CP for the past 2-3 days. To activate the cath lab?

The Initial ECG in Today’s CASE:

The rhythm in ECG #1 is sinus at 65-70/minute. Intervals (PR - QRS - QTc) are all within normal limits. The axis is slightly leftward (at about -10 degrees — as suggested by slight negativity of the small amplitude QRS in lead aVF — but not negative enough to qualify as LAHB, because the QRS in lead II is all positive).

• Voltage for LVH is easily satisfied in many leads (Very tall R wave in lead I — R in lead aVL ~20 mm [given overlap with the S wave in lead aVR] — deep S waves in V1,V2 + tall R waves in V5,V6 ≥35 mm). 
• For more regarding ECG criteria for LVH — See the ADDENDUM below and/or ECG Blog #73 and ECG Blog #245.

Regarding Q-R-S-T Changes:

• Q Waves — Tiny normal septal q waves in leads I,aVL.
• R Wave Progression — Normal R wave progression — with appropriate transition (where the R wave becomes taller than the S wave is deep) occurring between leads V3-to-V4.
• ST-T Wave Changes — There is ~1 mm of lateral J-point ST depression, with coving of ST segments and deep symmetric T wave inversion (seen in leads I,aVL; V4,5,6). There is 1-2 mm of ST elevation in leads III,aVF and V1 — with the T waves in leads III and aVF being disproportionately tall and "bulky" (with a mirror-image opposite appearance to the J-point depression and deep T wave inversion seen in lateral leads). 

MY Impression of ECG #1:

As a single tracing in a patient with 2-3 days of CP — this is a difficult ECG to interpret. My thoughts were as follows:

• The rhythm is sinus. Marked LVH is suggested by greatly increased QRS amplitude in multiple leads in this patient with longstanding hypertension (See Figure-3 in the ADDENDUM below for the ECG criteria for LVH that I favor).
• My written interpretation on a tracing such as this one would read, "Marked LVH and 'strain' and/or ischemia — with need for clinical correlation." 
• Pure LV "strain" tends to produce downsloping ST depression with asymmetric T inversion in ≥1 of the lateral leads (ie, leads I,aVL; V5,V6). Although it is not uncommon in patients with marked hypertension to see deep, symmetric T wave inversion in lateral leads — pure LV "strain" is generally not associated with ST coving, as is clearly seen in lead V4 of ECG #1 (See Figure-4 below in the ADDENDUM for the ECG picture of typical LV "strain" ).
• In addition — the ST elevation in leads III and aVF, in association with the hypervoluminous T waves in these leads — is not expected with pure LV "strain".
• On the other hand — the ST elevation seen in lead V1 is perfectly consistent with LVH and LV "strain" (ie, The shape of this ST-T wave in lead V1, in association with the deep S wave in this lead — is a mirror-image opposite picture of the typical expected appearance of LVH with "strain" in a lateral chest lead).
• 
  
• BOTTOM Line: Today's patient presented with a 2-3 day history of chest pain and the ECG shown in Figure-1. While this initial ECG is not diagnostic of an OMI (ie, of acute coronary Occlusion) — there are enough findings present in ECG #1 that are not expected with simple LVH and "strain", such that further evaluation is clearly indicated.

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The CASE Continues:

The first 2 high-sensitivity troponin values returned slightly elevated. A prior ECG from 9 years earlier was found. For ease of comparison — I have put this patient's baseline tracing and his initial ECG in today's case together in Figure-2.

• Does seeing this patient's "baseline" ECG change your interpretation of ECG-1?

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

Comparison of the 2 ECGs in Figure-2:

Availability of a prior tracing on today's patient confirms that all of the ST-T wave abnormalities described above for ECG #1 — are new compared to this patient's baseline tracing done 9 years earlier.

• Limb lead QRS amplitudes have greatly increased since the ECG baseline done 9 years earlier.
• Given the large amplitude of the QRS complex in lead V2 of ECG #2 — I found it hard to determine if overall chest lead amplitude was changed.
• There was no ST elevation and no hypervoluminous T waves in leads III and aVF of ECG #2 that was done 9 years earlier.
• There was no J-point depression — no ST segment coving — and no T wave inversion on the prior ECG.
• 
  
• BOTTOM LINE: ECG changes of LV "strain" and/or ischemia that we see on today's initial ECG — were not present 9 years earlier. That said — We have no idea when during this 9-year interim period these abnormal ST-T wave findings may have developed.

CASE Follow-Up:

In view of this patient's CP at the time he was seen in the ED — the 2 slightly elevated troponin values — and the abnormal ST-T wave findings on the initial ECG (with all of these ST-T wave changes being new since the baseline ECG done 9 years earlier) — Cardiac cath was performed.

• Cardiac cath showed normal coronary arteries.
• Cath pictures and the formal Echocardiogram indicated apical HCM (Hypertrophic CardioMyopathy) as the probable etiology of the abnormal ECG in Figure-1.

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COMMENT:

To emphasize —  Cardiac catheterization was completely appropriate in today's case — as today's patient presented with ongoing CP over the 2-3 days before he arrived in the ED — troponin was elevated (albeit modestly) — and his initial ECG did show ST-T wave changes that suggested "something more" than simple LVH (albeit not being overly suggestive of acute coronary occlusion).

• Taking another LOOK at today's initial ECG (and secure with the knowledge from cardiac catheterization that today's patient does not have an acute OMI [ = Occlusion-based MI] — but instead has apical HCM) — the ECG in Figure-1 is completely consistent with this diagnosis! 
• ST-T wave changes in Figure-1 are localized to lateral leads (ie, leads I,aVL; and V4,5,6) — especially in leads with increased QRS amplitude. In contrast — with LAD occlusion, there is usually at least modest associated ST elevation in lead aVL (and often also in lead I).
• There is no loss of R wave in anterior leads in Figure-1 (as opposed to poor R wave progression that is commonly seen with LAD OMI).
• The ST-T wave picture in lead V1 of Figure-1 is typical of LVH with "strain" (ie, It is the mirror-image opposite picture of what lateral chest leads typically show with marked LVH).
• Rather than Wellens' T waves — the most abnormal appearing chest lead ( = lead V4) is much more suggestive of a transitional (repolarization) change from the positive ST-T waves in leads V1,2,3 — "on the way" to ST coving and deep T wave inversion seen in the remaining chest leads. Like recognition of a face that you know, but have trouble describing in words — this appearance does not suggest OMI.
• 
  
• P.S.: An additional reason justifying prompt cardiac cath in today's case — is how different the initial ECG in Figure-1 looked compared to the "baseline" ECG on file. It would be interesting to see what an Echo from 9 years earlier looked like — but we do not know if such a study was previously done. It therefore appears that this patient's apical HCM continued to evolve over this 9 year period (rendering it impossible to be certain that ST-T wave abnormalities in Figure-1 were all attributable to apical HCM and not acute ischemia).

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About HCM (Different Forms of this Entity):

I've excerpted what appears below from My Comment in the December 26, 2023 post in Dr. Smith's ECG Blog.

HCM is an "umbrella term" applied to the presence of LVH in the absence of "abnormal cardiac loading conditions" (Hughes et al — JAHA 9:e015294, 2020). These are often felt to be the result of autosomal dominant mutations in sarcomeric protein genes — and may present with a number of distinct LVH forms, including the "classic" = asymmetric septal hypertrophy form (which is the type most commonly referred to when the abbreviation "HCM" is used) — concentric HCM — reverse septal — neutral — and apical HCM (initially known as Yamaguchi Cardiomyopathy — and sometimes abbreviated as ApHCM ).

• Clinically — Overall management of the above different morphological forms of HCM is similar for the emergency provider. That said — distinction between "classic" HCM vs the apical HCM form may be useful because: i) ECG findings tend to be different (Lyon et al — Europace 20:102-112iii, 2018); — ii) Echo appearance is different when hypertrophy localizes to the apex; and, iii) There is a significantly greater incidence of AFib with apical HCM.
• 
  
• Beyond the scope of this ECG Blog — specific formal Echo findings may help to sort through the large "spectrum" of HCM disorders — encompassing "lower risk" HCM (in those with modest or moderate hypertrophy — but without obstruction) — vs higher-risk obstructrive forms of HCM.

ECG Findings with HCM:

Most patients with HCM do not have a normal ECG. Among the many ECG findings that may be seen in patients with "classic" HCM are the following:

• Increases in QRS amplitude.
• Large septal Q waves (Sometimes known as "dagger" Q waves — because these are deep but narrow Q waves seen in lateral leads). 
• Tall R wave in lead V1 and/or early transition in the chest leads (reflecting increased "septal" forces).
• Abnormal ST-T wave abnormalities.
• Conduction defects (ie, LBBB, IVCD).
• WPW 
• Cardiac arrhythmias (including AFib). 
• 
  
• The Problem: None of the above ECG findings are specific for HCM. The variety of potential ECG findings with "classic" HCM is great — which poses problems when contemplating whether or not to use the ECG as a screening tool in athletes.

ECG Findings with Apical HCM:

Apical HCM makes up a minority of patients who qualify as having "HCM" (ie, less than 10% in the non-Asian population). 

• With the exception "dagger" Q waves (which are typically a result of a thickened septum) — any of the other ECG findings listed above for "classic" HCM may be seen with apical HCM.
• The ECG finding that is most characteristic of apical HCM is the presence of Giant T waves. Although T wave inversion in ECG #1 is prominent — it is not quite deep enough to qualify as true "Giant" T waves (See ECG Blog #276 and ECG Blog #309).

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NOTE: For more on HCM, with a summarizing Table on the treatment approach to this group of disorders — Please check out My Comment in the October 28, 2023 post in Dr. Smith's ECG Blog.

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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 (outlined in Figures-2 and -3, and the subject of Audio Pearl MP-23 in Blog #205).
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• ECG Blog #209 — and ECG Blog #254 — Reviews a case of marked LVH that results in similar ST-T wave changes as may be seen with Wellens' Syndrome.
•  
• ECG Blog #245 — Reviews the ECG diagnosis of LVH.
• 
  
• ECG Blog #276 — and ECG Blog #309 — Reviews the entity of Giant T waves.

• 
  
• ECG Blog #73 — Reviews "My Take" on the ECG Diagnosis of LVH. 
• ECG Blog #92 — Presents another perspective for ECG Diagnosis of LVH.
•  
• The November 4, 2018 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) reviews 3 ECG Clues for rapid recognition of erroneous lead V1,V2 placement. 
• The March 31, 2019 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) illustrates the potentially misleading effect the pre-hospital ECG may have in patients with LVH, by cutting off S wave voltage in the anterior leads. 
• The March 29, 2019 post in Dr. Smith's ECG Blog — My Comment regarding Tracing A (at the bottom of the page) illustrates how LVH is a common mimic of acute ischemia. 
• The December 27, 2018 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) illustrates a case with anterior ST elevation from LVH that may falsely suggest acute anterior infarction.

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ADDENDUM (1/13/2024):

I've added below in Figure-3 and Figure-4 additional material to facilitate ECG diagnosis of LVH and LV "strain".

 

—  —

ECG Media PEARL #59 (9:10 minutes Audio) — Reviews the ECG diagnosis of LVH (and its impact clinically with both chronic and acute cardiac disorders).

Figure-3: The voltage and other criteria I favor for ECG diagnosis of LVH (Please see ECG Blog #73 for additional details).

Figure-4: ST-T wave appearance of normal (A) — vs "strain" (C) or a strain "equivalent" pattern (B) — vs ischemia (D). (Please see ECG Blog #73 for additional details).

ECG Blog #411 — Is it Wenckebach?

How would YOU interpret the tracing in Figure-1 — that was sent to me without additional information?

QUESTIONS:

• What is the rhythm?
• Is there AV dissociation? If so — WHY?
• 
  
• Clinically — HOW would you approach interpretation of this tracing in optimal time-efficient fashion?

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

KEY Clinical Point:

If I was the medical provider charged with the care of the patient whose ECG is shown in Figure-1 — I would approach this tracing in the following sequential stages:

• I’d first establish that the patient was hemodnamically stable with this ECG and this cardiac rhythm. Assuming this patient is at least momentarily stable — I’d then proceed as follows:
• 
  
• I’d take a quick look at the long lead rhythm strip. 
• To EMPHASIZE: The rhythm shown in the long lead II (below the 12-lead tracing in Figure-1) is not a simple arrhythmia — so rather than trying to come up with a precise interpretation of the rhythm — I’d spend no more than 5-to-10 seconds to ensure there is a reasonable, stable-looking heart rate (which there is in Figure-1 — as the rhythm is supraventricular [narrow QRS everywhere] — some P waves are seen — and, a pattern of repetitive group beating (groups of 3 beats), with an average heart rate in the 60-80/minute rate range — appears to be present).
• 
  
• I’d then spend no more than 5-to-10 seconds looking at the rest of the 12-lead ECG to ensure that there is no ongoing emergency in need of immediate care (ie, No acute MI; No hyperkalemia, etc.).

COMMENT:

While I always advocate a systematic approach to both rhythm and 12-lead ECG interpretation — optimal clinical ECG interpretation entails prioritizing those parts of the tracing in front of you that mandate your immediate attention. Later, when you have a moment of time — You can complete your systematic assessment.

• With Regard to the Cardiac Rhythm: Our initial 5-to-10 second assessment of the long lead II rhythm strip should be all that is needed at this instant in time — because this limited amount of time should still allow you to establish: i) That the patient is hemodynamically stable; and, ii) That the rhythm is supraventricular — with at least some P waves, a narrow QRS everywhere — and, an overall heart rate in the 60-80/minute range.
• 
  
• PEARL #1 (Advanced Point): The fact that the QRS complex is narrow, with at least some P waves — and a pattern suggesting group beating — should clue us into: i) The possibility of Wenckebach conduction! — and, ii) That we need to carefully inquire about recent chest pain, paying special attention to the rest of this 12-lead ECG (looking carefully for signs of acute or recent infarction — because AV Wenckebach is common with acute inferior MI). It is much easier to identify Wenckebach conduction IF you are looking for it!

Regarding the 12-Lead ECG:  

Applying the systematic approach I favor for 12-lead ECG interpretation (as detailed in ECG Blog #205):

• Rate & Rhythm: As stated above — there is a regular, supraventricular rhythm with some P waves, group beating, and an acceptable overall ventricular rate between ~60-80/minute.
• Intervals (PR-QRS-QTc): The PR interval varies — the QRS is narrow — the QTc looks normal (Best seen in leads V2,V3). 
• Axis: Normal (about +60 degrees).
• Chamber Enlargement: Depending on age of the patient — voltage for LVH may be present (ie, Deepest S in V1,V2 + tallest R in V5,V6 ≥35 mm — IF the patient is ≥35 years of age).

Regarding Q-R-S-T Changes: 

• Q waves: Small q waves of uncertain significance are seen in the inferior leads.
• R Wave Progression: Normal, with transition (where height of the R wave becomes taller than the S wave is deep) — occurs normally, here by lead V4.
• ST-T wave Changes: Show some nonspecific ST-T wave flattening, and perhaps shallow T wave inversion in lead aVL. The slight amount of ST elevation that we see in lead V2 is common and normal.
• 
  
• Clinical IMPRESSION: The ECG in Figure-1 shows nonspecific ST-T wave abnormalities — but nothing that looks acute.

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Looking Closer at the Rhythm in Today's CASE:

As reviewed in ECG Blog #185 — I favor the Ps, Qs, 3R Approach for systematic, time-efficient interpretation of the cardiac rhythm.

• PEARL #2: When looking for P waves — I find it easiest to first identify those P waves that I am certain about. I have done this with RED arrows in Figure-2.
• The presence of multiple, regularly-spaced RED ( = definitely present) P waves in Figure-2 suggests: i) that there is a very good chance that the underlying atrial rhythm will be regular throughout the long lead II rhythm strip; and, ii) that the P-P interval between any 2 consecutive RED arrows will clue us in to where the remaining (partially hidden) P waves can be found. 
• Use of calipers can facilitate confirming that the underlying atrial rhythm in Figure-2 is in fact regular. With calipers — it takes only seconds to confirm this!
• PINK arrows highlight that the on-time beginning little "hump" at the very onset of the QRS of beats #2 and #5 clearly represents 2 additional on-time P waves.
• Completion of our "P wave search" can then be easily accomplished by noting the subtle-but-unmistakeable distortion under the PURPLE arrows toward the end of the T waves of beats #1 and 4 — and at the very onset of the QRS of beats #8 and #11.

Figure-2: I've labeled atrial activity in today's tracing with colored arrows (See text).

PEARL #3: Recognition that true group beating is present, in association with an underlying regular atrial rhythm — strongly suggests there is some type of 2nd-degree AV block in which there is Wenckebach conduction (ie, the presence of an underlying regular P wave rhythm is an essential component of the typical forms of AV block). 

• Focus on this concept facilitates recognizing the 3 true groupings in Figure-3 (within the dotted WHITE rectangles). Note the uncanny similarity in duration of the R-R interval between the first 2 beats in each group (ie, the R-R interval between beats #2-3; 5-6; and 8-9) — as well as for the R-R interval between the last 2 beats in each group (ie, the R-R interval between beats #3-4; 6-7; and #9-10) — as well as for duration of the R-R intervals of the short pauses that separate each of the groups (ie, the R-R interval between beats #1-2; 4-5; 7-8; and 10-11). This amount of symmetry for the relative duration of R-R intervals within each group of beats is not the result of chance!

Figure-3: RED arrows highlight that the atrial rhythm in the long lead II rhythm strip is regular. Note the 3 true groupings (within the dotted WHITE rectangles).

PEARL #4: We know that there is at least transient AV Dissociation in today's rhythm — because the PR interval of some on-time sinus P waves is clearly too short to be able to conduct (ie, Despite their on-time occurrence — the WHITE arrow P waves before beats #2,5,8 and 11 in Figure-4 — do not have enough time for normal conduction through the AV node).

• Since beats #2,5,8 and 11 all manifest a narrow QRS complex — and are not preceded by sinus P waves with a realistic chance of conducting — this means that these 4 QRS complexes are junctional beats.
• Note that each of these beats is preceded by a similar R-R interval of just under 5 large boxes — which corresponds to an ever-so-slightly accelerated junctional escape rate of ~65/minute.
• That said — We have no idea if the WHITE-arrow P waves that appear at the onset of the QRS of beats #2,5,8 and 11 might possibly have conducted — IF they were given a chance to do so (ie, IF the junctional escape rate would have been slower than 65/minute).

PEARL #5: Despite the presence of at least transient AV dissociation — the rhythm in  Figure-4 is not complete AV Block.

• Most of the time when there is complete AV block — the escape rate (be this a junctional or ventricular escape rhythm) will be regular. The obvious irregularity of the ventricular response in Figure-4 — immediately tells us this is not complete AV block.
• QRS complexes that occur earlier-than-expected are likely to be conducted beats! (ie, Beats #4,7 and 10 in Figure-4 are therefore likely to be conducted — and beats #3,6,9 and 12 may also be conducted).

PEARL #6: As per PEARL #4 — we have already established that there is transient AV dissociation in Figure-4 (because beats #2,5,8,11 are clearly not conducted). There appear to be 2 reasons for this transient AV dissociation in today's rhythm:

• As reviewed in ECG Blog #192 — the 3 Causes of AV Dissociation are: i) Default; ii) Usurpation; and, iii) Some form of 2nd- or 3rd-degree AV block. 
• Today's tracing is interesting — in that the reason for transient AV dissociation (ie, non-conduction of the WHITE-arrow P waves in Figure-4) — appears to be a combination of the slightly accelerated junctional beats (beats #2,5,8 and 11) — and the 2nd-degree AV block that leads to the slight pauses after beats #1,4,7 and 10.

PEARL #7: Looking closer in Figure-4 at the P waves in each of the 3-beat groupings — tells us that there is 2nd-degree AV block, Mobitz Type I ( = AV Wenckebach) because of the following findings:

• As already stated — the WHITE-arrow P waves in each group do not conduct to the ventricles — because the PR interval is too short.
• That said — We know that the next P wave in each grouping (ie, the light BLUE-arrow P waves) — does conduct to the ventricles, because the PR interval preceding beats #3,6,9 and 12 are all equal!
• This is followed by the dark BLUE-arrow P waves that are also conducting — but with slight increase in the PR interval compared to the light BLUE PR interval. Once again — We know that the dark BLUE-arrow P waves are conducting — because the PR interval preceding beats #4,7 and 10 are all equal!
• The last P wave in each grouping (ie, the YELLOW-arrow P waves) — are non-conducted — thus completing the AV Wenckebach cycle of progressive PR interval lengthening until a beat is dropped.
• 
  
• Additional typical features of AV Wenckebach in Figure-4 include: i) The narrow QRS (Mobitz II usually has a wide QRS — because of its origin at a lower point in the conduction system); ii) Progressive shortening of the R-R interval within groups (the R-R intervals between beats #3-4; 6-7; and 9-10 — are shorter than the R-R intervals between beats #2-3; 5-6; 8-9); and, iii) The pause containing the dropped beat is less than twice the shortest R-R interval.

Figure-4: I've colored the P waves from Figure-3 (See text).

SUMMARY:

The rhythm in today's case is sinus (ie, regularly-occurring P waves) — with 2nd-degree AV block, Mobitz Type I ( = AV Wenckebach). Each of the 3-beat Wenckebach groups begins with a slightly accelerated junctional beat (which results in transient AV dissociation).

• The overall ventricular rate in today's tracing should be sufficient at ~60-80/minute for adequate perfusion. 
• Although it is common for Mobitz I to be associated with acute inferior MI — the 12-lead ECG in today's case does not suggest any acute ST-T wave changes.

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LADDERGRAM:

To clarify the mechanism for today’s rhythm — I've derived a laddergram with step-by-step description of events. I begin with Figure-5.

• NOTE: For review of the Basics for HOW to read (and draw) laddergrams — See ECG Blog #188).   

Figure-5: The 1st step in laddergram construction — is to represent each of the P waves in the Atrial Tier. Since conduction through the atria is fast — vertical lines are used, drawn from each of the ARROWS that overlie P waves in this tracing.

Figure-6: Since all QRS complexes are narrow — each of the 12 beats in this tracing is supraventricular. Knowing this allows me to draw in conduction within the Ventricular Tier — which I represent with slightly inclined forward-directed lines with an arrow to indicate the downward direction of conduction. 
NOTE: I find Power Point optimal for drawing laddergrams — as it allows ready duplication of laddergram elements and precisely vertical displacement to ensure laddergram elements appear exactly below P waves and QRS complexes in the original rhythm strip.

Figure-7: It's now time to "solve" the laddergram. I begin by a survey of all P waves (RED arrows — which are represented by the RED vertical lines in the Atrial Tier) — and of all 12 QRS complexes (vertical RED lines within the Ventricular Tier) — with the goal of determining which P waves seem most likely to conduct to the ventricles.

Figure-8: "Armed" with the clue that the PR intervals preceding beats #3,6,9 and 12 look to be both normal and equal — I felt comfortable presuming that each of these BLUE-arrow P waves are conducting (which I illustrate with the slanted BLUE lines within the AV Nodal Tier that connect these P waves to the appropriate QRS complexes. 

Figure-9: I then connected the 2nd P wave in each group (highlighted by the dark BLUE arrows) — with the appropriate QRS complexes for beats #4,7 and 10 in the Ventricular Tier (slanted dark BLUE lines within the AV Nodal Tier). Note slight increase in the amount of slanting of these dark BLUE lines, reflecting slight increase in the PR interval since the light BLUE P waves conducted beats #3,6,9 and 12.

Figure-10: I next chose to represent the YELLOW arrow P waves — which clearly are not conducting because they are not followed by any QRS complexes (YELLOW butt ends drawn within the AV Nodal Tier). This left a limited number of P waves and QRS complexes unaccounted for ...

Figure-11: But the PR interval for the WHITE arrow P waves is clearly too short to conduct! (represented by WHITE butt ends drawn within the AV Nodal Tier).

Figure-12: Since neither the YELLOW nor WHITE arrow P waves are conducting — beats #2,5,8 and 11 have to be arising from the AV node! (The dotted RED lines with butt ends indicate retrograde conduction from the slightly accelerated junctional escape beats — that prevent WHITE arrow P waves from being conducted through the AV Nodal Tier).

Figure-13: My completed laddergram illustrating the mechanism for today's rhythm. There is 2nd-Degree AV Block, Mobitz Type I (AV Wenckebach) — in which slightly accelerated junctional escape beats produce 1 beat of AV dissociation until sinus conduction resumes with beats #3,6,9 and 12.

Final Advanced Point: 

Did YOU notice in Figure-13 — that the QRS of each of the junctional beats ( = beats #2,5,8 and 11) is slightly taller than the QRS of the remaining 8 beats on this tracing?

• The above subtle observation can sometimes be a very helpful clue that these slightly different-looking beats are not sinus-conducted — but instead arise from the AV Node.
• The reason escape beats from the AV Node sometimes look slightly different than sinus-conducted beats — is that the precise site of origin within the AV Node from where these beats arise may be slightly different than the path within the AV Node through which sinus-conducted beats pass.
• To Emphasize: This clue is not needed for us to know that beats #2,5,8,11 in today's tracing are junctional beats — since it is obvious that the P waves preceding beats #2,5,8,11 are too close to the QRS to be conducted. But there are times when it will not be readily apparent if a given QRS complex represents a sinus-conducted beat vs junctional escape — in which case, the observation that QRS morphology differs slight may reveal which beats are junctional escape beats (See ECG Blog #63 — for a clinical example of this phenomenon!).

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Acknowledgment: My appreciation to ไกรสร เต็ง (from Bangkok, Thailand) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #185 — Reviews my System for Rhythm Interpretation, using the Ps, Qs & 3R Approach.
• ECG Blog #205 — Reviews my System for 12-Lead ECG Interpretation.
• 
  
• ECG Blog #245 — Reviews ECG diagnosis of LVH.
• 
  
• ECG Blog #188 — Reviews how to read and draw Laddergrams (with LINKS to more than 90 laddergram cases — many with step-by-step sequential illustration).
• 
  
• ECG Blog #192 — The 3 Causes of AV Dissociation.

• ECG Blog #191 — Reviews the difference between AV Dissociation vs Complete AV Block.
• 
  
• ECG Blog #389 — ECG Blog #373 — and ECG Blog #344 — for review of some cases that illustrate "AV block problem-solving".
• 
  
• ECG Blog #63 — Reviews a case of 2nd-Degree AV Block, Mobitz Type I with Junctional Escape Beats.
• ECG Blog #267 — Shows step-by-step Laddergrams, with derivation of a case of Mobitz I with more than a single possible explanation.
• 
  
• ECG Blog #404 (ECG Video) — applies the Ps,Qs,3R Approach to a case of 2nd-degree AV Block ( = Mobitz I or Mobitz II or Neither).
• ECG Blog #405 (ECG Video) — applies the Ps,Qs,3R Approach to a case of AV Dissociation vs Complete AV Block (What's the difference?).

 

ADDENDUM (1/6/2024):

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.

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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.

• Section 2F (6 pages = the "short" Answer) from my ECG-2014 Pocket Brain book provides quick written review of the AV Blocks.
• 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!

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ECG Media PEARL #75 (6:10 minutes Audio) — Reviews how to tell IF a Junctional (AV Nodal) Rhythm is pathologic or appropriate?