ECG Blog #166 (ST-T – AFib – LVH – SVT)

The ECG that appears in Figure-1 was obtained from a 65-year old woman who presented in acute heart failure (HF). She was on multiple medications. She was short of breath — and had been having intermittent chest discomfort.

• How would you interpret this ECG?
• Is it surprising that this patient presented in HF?
• What might account for the ST-T wave changes that are seen in many leads on this tracing?

Figure-1: 12-Lead ECG obtained from a 65-year old woman who presented in acute HF (See text).

Descriptive Analysis of the ECG in Figure-1: 
The rhythm is rapid and irregularly irregular. No P waves are seen in any of the leads. This defines the rhythm as AFib (Atrial Fibrillation) — seen here with a rapid ventricular response. Since most R-R intervals look to be a little less than 2 large boxes in duration — the average ventricular rate is over 150/minute (probably ~160-180/minute range).

• Intervals — The QRS complex is of normal duration. (The PR interval is not relevant when the rhythm is AFib — and the QTc interval is meaningless at as fast of a rate as seen here.).
• Axis — The mean QRS axis is normal (between +60-70 degrees).
• Chamber Enlargement — There is LVH (Left Ventricular Hypertrophy). The sum of the deepest S in V1,V2 + tallest R in V5,V6 ≥35 mm (Criteria for LVH used in this case are discussed in more detail below! ).

Looking next at Q-R-S-T Changes:

• Q Waves — No Q waves are seen.
• R Wave Progression — Transition is normal (occurs between lead V2-to-V3, albeit the R wave is already fairly tall by lead V2).
• ST-T Wave Changes — As an overall assessment, there is ST segment “scooping” and/or slight depression in multiple leads. We would describe this as diffuse NS (Non-Specific) ST-T wave abnormalities.

Figure-2: Common causes of ST-T wave depression (See text).

Clinical Impression / Clinical Notes: The rhythm is rapid AFib. In patients with new-onset AFib — loss of the atrial "kick" and the rapid ventricular response that so often accompanies new AFib (which significantly reduces the period of diastolic filling) — are reasons why new-onset HF and AFib are so commonly associated!

• Of interest in Figure-1 — Note the marked change in appearance of the QRS complex from beat-to-beat in lead aVL. This most likely reflects respiratory variation in this acutely ill patient with heart failure.
• As noted earlier — there is LVH.
• There are diffuse, nonspecific ST-T wave abnormalities that may be due to i) LV "Strain"; ii) Ischemia; iii) Drug effect; iv) Electrolyte Disturbance; v) Tachycardia; and/or, vi) Any combination of the above (Figure-2).

BOTTOM Line: There is rapid AFib — which is presumably new. That said — at least the ST-T wave changes that we see in Figure-1 do not appear to be acute in this patient with intermittent chest discomfort (ie, other than lead aVL — there is no ST elevation). Clinical correlation will be needed to determine which of the causes of ST-T wave depression that are listed in Figure-2 are likely to be operative in this case.

Looking closer at the ECG diagnosis of LVH in Figure-1:

• There are numerous criteria in the literature for ECG diagnosis of LVH. For simplicity — we summarize the criteria we favor in Figure-3. We discuss this topic fully in ECG Blog #73.
• In my opinion — there is an “art” to the ECG diagnosis of LVH. Clinical factors — including patient age, race and the presence of certain underlying heart diseases (such as longstanding hypertension or heart failure) predispose a patient to LVH. As a result — even when numerical criteria for LVH voltage fall slightly shy of the lower LVH voltage threshold — “probable” LVH can still be strongly suspected in an older adult with underlying heart disease, especially if ST-T wave changes of LV “strain” (or a “strain” equivalent) are present.
• To facilitate application of Figure 3 — We’ve counted R wave and S wave amplitude in several key leads for the ECG in this case, which we show in Figure-4. Voltage criteria for LVH are satisfied in this case by: i) Sum of the S in V1 (16 mm) + R in V5 (21 mm) ≥35 mm; and, ii) Sum of the R wave in lead II ≥20 mm.

Figure-3: Criteria we favor for the ECG diagnosis of LVH — excerpted from ECG Blog #73. NOTE — Only 1 voltage criterion need be met for LVH by voltage to be satisfied (See text).

Figure-4: We’ve counted R wave and S wave amplitude from Figure-1 in several key leads. Applying criteria suggested in Figure-3 — voltage for LVH is satisfied (See text).

Looking closer at the 6 Common Causes of ST-T Wave Depression from Figure-2:

• There are actually over 50 causes of ST-T wave changes on ECG. Although many of these causes are cardiac-related — there are also many that are not cardiac-related. Among the many non-cardiac causes of ST-T wave changes are hyperventilation; temperature extremes (excessive heat or cold exposure); anxiety or emotional stress; anemia; tachycardia; sleep deprivation; pulmonary disease; electrolyte abnormalities; central nervous system disorders; certain medications; and severe medical illness (among others). BOTTOM Line: Rather than attempting to commit to memory an exhaustive list of conditions that may predispose to ST-T wave changes — it suffices to appreciate the variety of entities that may produce changes on ECG. Remember: Many of these conditions are non-cardiac.
• NOTE: In general — causes of T wave abnormalities (including T wave flattening or frank T wave inversion) are similar to potential causes of ST segment depression.
• PEARL #1: The purpose of formulating the short list that we show in Figure-2 — is that it simplifies your task as the interpreter. As soon as you recognize generalized ST-T wave changes on an ECG — Consider this short LIST. Often — more than a single cause will be operative. For example — the patient in this case was an older woman on multiple medications, who presented in heart failure. As a result — she might be taking Digoxin and/or a Diuretic (which might contribute to electrolyte disturbance). She has heart failure and voltage for LVH — so the ST-T wave changes may reflect LV “strain” (or a strain equivalent). In addition, the ST-T wave changes we see in Figure-1 could reflect ischemia in this patient with intermittent chest discomfort. Finally, the very rapid ventricular rate may be contributing to ST-T wave flattening and depression that will resolve once the rate slows. BOTTOM Line — All of the potential causes of ST-T wave depression listed in Figure-2 may be contributing in varying degree to the ECG picture we see in Figure-1.

PEARL #2: The Shape of the ST-T wave may suggest which one (or more) of the 6 entities in our LIST is (are) most likely to be operative in a given patient (See bottom half of Figure-2):

• Ischemia — is suggested by symmetric T inversion (RED arrow in Panel B) — especially when seen in two or more leads of a given lead group (ie, in leads II, III and aVF — or in both leads I and aVL).
• Strain — from LVH, is suggested by asymmetric ST depression occurring in one (or more) of the lateral leads (less often in the inferior leads). Note the initial slow sagging of the ST segment with LV “strain” (BLACK arrow in Panel A) — with more rapid return to the baseline. “Strain” is more likely to be the cause of ST depression when voltage for LVH is present — although occasionally, there may be ST-T wave changes suggestive of “strain” without accompanying voltage.
• "RV strain" — is suggested IF the picture in Panel A of Figure-2 is seen in right-sided leads (leads II,III,aVF; or V1,V2,V3) in a patient with RVH.
• Use of Digoxin may affect ST-T waves in one of 3 ways: i) There may be “scooped” ST depression in multiple leads (that simulates an inverted ice cream cone, as in Panel D of Figure-2); or, ii) Digoxin “effect” may produce a "strain"-like pattern (identical to Panel A); or, iii) Despite use of an appropriate amount of  Digoxin — there may be little-to-no effect on the ST-T wave. In my experience (from correlating ECG ST-T wave appearance to serum Digoxin levels over many years) — the serum Digoxin level correlates poorly with the amount of ST-T wave scooping or depression. Thus, despite even high serum Digoxin levels — some patients fail to manifest ST-T wave abnormalities — whereas other patients show marked ST-T wave changes despite surprisingly low serum Digoxin levels.
• Finally — Panel C in Figure-2 shows a non-specific ST-T wave pattern, in which the T wave and ST segment are flattened (if not slightly depressed). This pattern is called “nonspecific” — because any of the many potential causes of ST-T wave abnormalities may be operative.
• BOTTOM Line (regarding ST-T wave changes in Figure-1) — The depressed ST segments manifest a scooped appearance in many leads. We therefore need to find out IF this patient who is on multiple medications (and who is in heart failure) is taking Digoxin? That said — any (or all) of the causes listed in Figure-2 may be contributing to the ST-T wave changes that we see in Figure-1.

ECG Blog #165 (MI - Acute - Old - Unknown Age - Aneurysm - Fragmentation)

Imagine you are overreading tracings that were done in an ED (Emergency Department). Unfortunately, you have NO clinical information on the patient whose ECG is shown in Figure-1.

• How would you interpret this ECG?
• Clinically — What do you suspect is going on with this patient?

Figure-1: 12-Lead ECG obtained from a patient who presented to the ED. Unfortunately — NO clinical information is available. How do you interpret this tracing? (See text).

Descriptive Analysis of the ECG in Figure-1:
An upright P wave with a normal PR interval is seen in lead II. The ventricular rhythm is fairly regular — and the QRS complex is not widened (ie, not more than 0.10 second) — therefore, this is a sinus rhythm at ~60-65/minute.

• All intervals are normal (ie, the PR interval is not more than 1 large box in duration — the QRS not more than 1/2 a large box — and the QT not more than 1/2 the R-R interval).
• There is a markedly leftward axis (ie, the QRS is predominantly positive in lead I — but all negative in lead aVF).
• There is no chamber enlargement.

The main abnormalities are in assessment of Q-R-S-T Changes:

• Q Waves — Small and narrow q waves are seen in leads I and aVL. Entirely negative QS complexes are seen in leads II, aVF; and V2, V3. Larger and/or wider-than-expected Q waves are seen in leads V4, V5 and V6.
• R Wave Progression — Transition is slightly delayed, since the R wave does not become taller than the S wave is deep until between leads V4-to-V5. NOTE: There is an initial positive deflection (r wave) in lead V1. This small initial r wave is then lost as the fragmented and entirely negative QS complex in lead V2 forms (ie, there is “Loss of R Wave” as we move from lead V1-to-V2).
• ST-T Wave Changes — There is nonspecific ST-T wave flattening in lead aVL. There is straightening of the ST segment takeoff in several anterior leads (slanted BLUE lines in Figure-2). Slight ST elevation is seen in lead V1 — and then 2-3 mm of J-point ST elevation is seen in leads V2, V3 and V4 (small PURPLE arrows above the dotted RED line baseline).
• Other Findings — There is fragmentation of the QRS that deforms the downslope of the S wave in a number of leads (small BLUE arrows).

Figure-2: We’ve labeled Figure-1. Small BLUE arrows highlight fragmentation. Slanted BLUE lines indicate straightening of the ST segment takeoff in several leads. The dotted RED lines with small PURPLE arrows indicate the amount of ST elevation in several anterior leads (See text).

Clinical Impression /Clinical Notes: As stated — We were not provided with any clinical information, other than that this patient presented to the ED.

• The rhythm is sinus at ~60-65/minute.
• Marked left axis deviation is present. It is difficult to determine if the reason for this is: i) LAHB (Left Anterior Hemi-Block); ii) Inferior MI of uncertain age; and/or, iii) Both LAHB + prior Inferior MI.
• Identification of fragmentation (ie, irregularities) in one or more QRS complexes (small BLUE arrows) suggests scarring — that may be the result of prior infarction, cardiomyopathy, or some other form of structural heart disease. Such fragmentation does not tell us whether heart disease is acute or has been present long-term — but it nonetheless is an invaluable clue for conveying that the patient in question almost certainly has some form of underlying structural heart disease.
• Returning to assessment of the inferior leads — the finding of fragmentation (irregularity) of S wave downslope in lead aVF — and especially the QRS shape in lead II (which suggests an initial Q wave, that is aborted by a small positive deflection that fails to reach to baseline, before continuing on as a deep S wave) — strongly suggests that there has been inferior MI at somepoint in time. Lack of any inferior lead ST elevation + the nonspecific ST-T wave flattening in lead aVL suggest this to be an old inferior MI.
• Finally — the small, thin initial r wave in lead III is against inferior MI, and strongly suggests LAHB.
• “My Take” — Inferior MI and LAHB are “competing” conditions — in that the presence of one may mask the other. Given the conflicting ECG findings described above — I strongly suspect that there is both LAHB + old inferior MI.

Assessment of Chest Leads in Figure-2: We can say with some certainty that extensive Anterior MI has occurred at some point in time because: i) As noted above — there is Loss of r Wave in going from lead V1-to-V2; ii) Deep QS complexes are seen in leads V2 and V3; and, iii) Deep Q waves continue in leads V4 and V5 — and the Q wave in lead V6 is wider-than-expected for a “septal” Q wave.

• Preservation of the initial r wave in lead V1 suggests (at least in theory) — that the septum remains intact (it is the initial left-to-right vector of septal depolarization that produces the initial r wave in lead V1; This is lost with septal infarction). We would therefore describe the location of the MI in Figure-2 as “anterior” or “antero-lateral” — but not “antero-septal” (because the initial r wave in lead V1 is preserved).

In contrast to the picture in the inferior leads (in which we see Q waves in leads II and aVF — but no ST elevation) — there is significant ST elevation that begins in lead V1, and attains 2-3 mm in leads V2-thru-V4. This raises the QUESTION of whether the Anterior MI in Figure-2 is: i) new or recent?; ii) old?; or perhaps: iii) an “old” MI with superimposed new or recent injury?

• Finding a prior ECG on this patient could be of invaluable assistance in answering this question — since this will tell you which of the above ECG findings were previously present. But without a prior ECG — it is virtually impossible to be certain ...
• The History is extremely important! We were told that the ECG in Figure-2 was recorded in the ED — but we were not told if the patient was asymptomatic or having new-onset chest pain at the time ... IF the history for this patient did not sound like an acute MI — this would support the likelihood that the changes were not new.
• Repeating the ECG in the ED a little while later may help. An acute evolving STEMI tends to show evolution of ECG changes, sometimes over a surprisingly short period of time.
• Doing an Echo in the ED may help! Seeing a large LV (left ventricular) aneurysm with reduced or absent contractility would support chronicity rather than acute MI.

My HUNCH: I believe it most likely that extensive antero-lateral MI occurred in the past for the ECG shown in Figure-2 because: i) There is a lot of fragmentation (this usually though not always takes time to develop); ii) Considering that QS complexes and/or large Q waves occur in 5 of the 6 chest leads — the amount of ST elevation is relatively modest; and, iii) The ST segment takeoff in anterior leads shows straightening (slanted BLUE lines in Figure-2) — but lacks the coved ST segment appearance that is more characteristic of acute injury.

• BOTTOM Line: Clinical correlation will be needed to arrive at a definitive answer (ie, history; finding a prior tracing; serum troponin values, Echo, serial ECGs in the ED, etc.). That said — the KEY Points from this blog post are: i) To recognize ECG findings suggestive of new or recent vs old infarction; ii) To realize that you may not be able to “date” the infarction on the basis of a single ECG without clinical correlation; and, iii) To appreciate that the ECG picture seen in Figure-2 would be perfectly consistent with development of LV Aneurysm following extensive Anterior MI. 

ECG Blog #164 — PACs vs Wenckebach ... ?

The long lead II rhythm strip that appears in Figure-1 was sent to me without the benefit of clinical information. Unfortunately, no 12-lead ECG is available on this patient …

• How do you interpret the rhythm in Figure-1?
• Along the way to arriving at an ECG rhythm diagnosis — there are a bunch of observations that should be made. How many of these can you come up with?
• What little device that experts in rhythm interpretation routinely carry around — will be invaluable for evaluating this rhythm?

Figure-1: Long lead II rhythm strip. No history available. How do you interpret the rhythm? 

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• NOTE #1: This long lead II rhythm strip was recorded at the standard recording speed of 25 mm/second. Although there is slight distortion due to some angulation of the ECG grid — the quality of this tracing is more than adequate for interpretation.

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MY System for Rhythm Interpretation:

Once you have looked at your patient to assess for hemodynamic stability — there are 5 KEY Parameters to assess in the interpretation of any rhythm. These 5 parameters are easily remembered by the saying, "Watch Your Ps, Qs & the 3Rs". It does not matter in what sequence you assess these 5 parameters — and, we often alter the sequence in which we look for them, depending on the tracing at hand. The important thing, is to be certain you address each of these 5 parameters for every rhythm strip you encounter. LOOK FOR:

• P Waves (or better yet, for the presence or absence of atrial activity).
• QRS Duration (We consider anything more than half a large box in duration on ECG grid paper as “wide” [ = >0.10 second] ).
• Rate of the rhythm.
• Is the rhythm Regular?
• And, IF P waves are present — are P waves Related to neighboring QRS complexes? (ie, are P waves conducting?).

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• CLICK HERE — For more detailed explanation of my “Ps, Qs & 3R” Approach to Rhythm Interpretation. (If you click on SHOW MORE below this video on the YouTube page — You’ll see a detailed linked Contents of all that is contained in this video!).

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MY Approach to the Rhythm in Figure-1:

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The rhythm in Figure-1 is a complex tracing! I fully acknowledge to not being 100% certain of my final diagnosis. That said — I believe that by using a systematic approach, we can deduce the most likely answer. My step-wise approach for interpreting this tracing is as follows:

• Regarding assessment of Ps, Qs & the 3Rs parameters — the QRS complex is narrow — the ventricular rhythm is not regular — but, some P waves are present! It appears that at least some of these P waves are related to neighboring QRS complexes (More details on the P wave rhythm below). Since the QRS complex is narrow — the rhythm is supraventricular.
• Observation #1: There is group beating. This is most easily observed by stepping back a little bit from the rhythm in Figure-1. Thus, there are 3 groups of 2-beats each (beats #1-2; #6-7; and #8-9) — and 2 groups of 3-beats each (beats #3,4,5; and beats #10,11,12). Recognition of group beating is helpful — because it immediately tells us that some type of Wenckebach conduction may be present. 
• NOTE: There are other potential reasons for group beating — including atrial or ventricular bigeminy or trigeminy. That said — prompt recognition of group beating puts us on alert, and this facilitates and expedites recognition of a Wenckebach conduction disturbance when one is present.
• PEARL: BEFORE going any further — find a pair of CALIPERS! As is the case with other highly challenging arrhythmias — I predict that you will not be able to appreciate (or interpret) the fine points of this complex rhythm unless (until) you use calipers.

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Since we have established that the rhythm in Figure-1 is supraventricular and manifests group beating — the next KEY to rhythm assessment is a search to identify all signs of atrial activity.

• Observation #2: Start by looking for definite P waves — and, as we do so, we note that definite P waves are present! Definite P waves precede beats #1, 3, 6, 8, 10 and 13 (RED arrows in Figure-2). The PR interval preceding each of these beats is prolonged (ie, clearly more than 0.21 second) — and, this PR interval is the same in front of each of these beats. The fact that the PR interval preceding beats #1, 3, 6, 8, 10 and 13 is identical tells us that all of these beats are conducted, here with 1st-degree AV block.

Figure-2: We have added RED arrows to Figure-1 to highlight that each of these P waves is conducted with the same prolonged PR interval (See text).

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We continue to look for other signs of atrial activity in the rest of the rhythm strip:

• Observation #3: There appears to be notching in the ST segment of beats #2, 4, 7, 9 and 11 (YELLOW arrows in Figure-3). The fact that this notching occurs at approximately the same point in the ST segment of beats #2, 4, 7, 9 and 11 — but never appears in the ST segments of the 1st beat in each grouping (ie, there is no notching in the ST segment of beats #1, 3, 6, 8 and 10) — strongly suggests that this notching is not due to chance (and not due to artifact) — but instead, most likely represents additional atrial activity!

Figure-3: YELLOW arrows highlight consistent notching at the same point in the ST segment for the 2nd beat in each grouping. This notching indicates additional atrial activity (See text).

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Observation #4: There appears to be an underlying regular atrial rhythm (ie, a regular P-P interval) throughout the rhythm in Figure-3! This is not immediately apparent. We deduce the presence of a regular underlying atrial rhythm in the following manner.

• Common things are common. Since we know that each of the P waves highlighted by RED arrows is conducting in Figure-3 — and, since the distance between the YELLOW arrow and the RED arrow found in between beats #2-3; #7-8; and 9-10 looks to be equal — the most common (and logical) explanation for the colored arrows that we see in Figure-3, is that there must be an underlying regular P wave rhythm.
• This is where your CALIPERS come in! Set your calipers to the distance that separates the YELLOW and RED arrows that are found between beats #7-8. Then, IF you move this distance to the LEFT with your calipers — you will fall upon some extra peaking in the T wave of beat #6 (BLUE arrow in Figure-4). This extra peaking is the result of this next on-time P wave occurring at the same time that the T wave of beat #6 peaks (BLUE arrow in Figure-4).

Figure-4: Moving your calipers to the LEFT by an amount equal to the distance that separates the YELLOW and RED arrows between beats #7-8 — places you precisely on the extra peaking of the T wave of beat #6 (BLUE arrow). This extra peaking is the result of superposition of the next on-time P wave, that occurs at the same time that the T wave of beat #6 peaks (See text).

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• Keeping your calipers set to this precise distance — you can now walk out extra peaking in the T waves of beats #1, 3, 6, 8 and 10 — and, an extra subtle notch in the upslope of the T wave of beats #5 and 12 (BLUE arrows in Figure-5). For practical purposes — the regular colored arrows in Figure 5 confirm the presence of an underlying regular atrial rhythm (BLUE arrows).

Figure-5: There appears to be a regular, underlying sinus rhythm — with a consistent P-P interval between each of the arrows (See text).

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Observation #5: After establishing that the underlying atrial rhythm is regular — it becomes apparent that most of "the Footprints of Wenckebach" are present for the rhythm in Figure-5. This suggests that the rhythm is 2nd-Degree AV Block, Mobitz Type I ( = AV Wenckebach). These are the "Footprints" that we see:

• Group beating.
• Lengthening of the PR interval until a beat is dropped — after which the cycle resumes and the PR interval shortens.
• A regular atrial rhythm (ie, a regular, or at least fairly regular P-P interval).
• The pause that contains the dropped beat is less than twice the shortest R-R interval.
• Progressive shortening of the R-R interval within groups of beats, until a beat is dropped.

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PEARL ( = Beyond-the-Core): In addition to group beating — there are a number of other characteristics that suggest a periodicity consistent with some type of Wenckebach conduction. Marriott has colorfully labeled these characteristics as “the Footprints of Wenckebach”. We emphasize that Wenckebach conduction does not always manifest each of these findings — but recognition that several of these characteristics are present goes a long way toward suggesting the diagnosis!

• The best known of these “footprints” (and the easiest to spot) — is group beating. As we emphasized in Observation #1 — there are 3 groups of 2 beats, and 2 groups of 3 beats in Figure-5.
• Although Mobitz I, 2nd-degree AV block is defined by progressive lengthening of the PR interval until a beat is dropped — not every case of Wenckebach conduction “reads the textbook”. As we will see momentarily — this case is a little atypical — in that the PR interval increases between the 1st and 2nd beats in a group, but not between the 2nd and 3rd beats in a group.
• By definition — the atrial rhythm (P-P interval) should be regular (or at least almost regular) when there is AV block. I love this “footprint” — because recognition of significant irregularity in the underlying atrial rhythm is the best “tip-off” that you are dealing with something other than AV Wenckebach (ie, PACs, sinus pause or arrest, etc.).
• The last 2 “footprints” are not generally appreciated. The shortest R-R intervals in Figure-5 are the intervals between beats #4-5 and #11-12. It is easy to see with calipers that each of the pauses (ie, the interval between beats #2-3; #5-6; #7-8; #9-10; and #12-13) is less than twice the shortest R-R interval. This relationship is often not seen when the reason for group beating is sinus pauses or PACs.
• With Wenckebach groups that consist of 3-or-more beats — the R-R interval within the group tends to progressively decrease. The reason for this — is that the greatest increment (ie, increase) in PR interval with typical Wenckebach tends to be between the 1st and 2nd beats in the group. Thus, in Figure-5 — note that the R-R interval between beats #3-4 is greater than the R-R interval between beats #4-5. Similarly, the R-R between beats #10-11 is greater than that between beats #11-12. Appreciation of this relationship is especially helpful in recognizing Wenckebach conduction when there are no P waves (ie, with AFib) and with SA block. (NOTE: The R-R interval will not always progressively decrease within groups with Wenckebach conduction — but it is a helpful feature when it is present.).

Bottom Line: In the case of the rhythm shown in Figure-1 — my familiarity with looking for “the Footprints of Wenckebach” allowed me to suspect the diagnosis of this arrhythmia in less than 10 seconds! This is because I instantly recognized group beating — I next recognized definite conduction of the 1st beat in each group — and I saw what looked to be regularly-spaced notching and/or extra peaking that strongly suggested a regular underlying atrial rhythm. Confirming the regularity of this underlying atrial rhythm took mere seconds with use of calpiers — and these relationships, together with "the overall look" of this arrhythmia was enough to strongly suggest Wenckebach conduction to me.

• We devote our ECG Blog #236 to the 2nd-Degree AV Blocks. We highlight the "Footprints of Wenckebach", beginning at 1:20 minutes in the 15-minute Video Pearl on this blog post.

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CHALLENGE: PROVE to yourself how useful awareness of the “Footprints of Wenckebach” can be.

• How long does it now take you to suspect the correct rhythm diagnosis in our ECG Blog #55?

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Our Final Observation: It is possible for certain complex arrhythmias to have more than a single plausible rhythm interpretation. The way to PROVE that your interpretation is one of the plausible explanations — is to draw a Laddergram that makes sense, and which illustrates your theory.

• CONFESSION: It took me many years to become comfortable drawing laddergrams. The “good news” — is that it takes no more than a few minutes (and a little bit of practice) to become comfortable reading laddergrams. Our laddergram for the rhythm in this case is shown in Figure-6. Our explanation of events follows in the Figure legend.
• NOTE: For more on the basics of HOW to Read (and/or Draw) Laddergrams — Please see my ECG Blog #188 —

 

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Figure-6: Laddergram to illustrate our interpretation of this rhythm. RED arrows highlight the underlying regular atrial rhythm (schematically shown by the 18 short vertical RED lines in the Atrial Tier).

• The 1st beat in each group conducts with 1st-degree AV block and an identical PR interval (beats #1, 3, 6, 8, 10 and 13). 
• The 3 groups of 2 beats (ie, beats #1-2; #6-7; #8-9) manifest typical Wenckebach conduction — in that the PR interval increases until a beat is dropped. 
• The 2 groups of 3 beats (ie, beats #3,4,5; and #10,11,12) are slightly atypical — in that the PR interval preceding beats #5 and 12 is not longer than the PR interval preceding beats #4 and 11. I believe the reason for this discrepancy is simply due to the disproportionately large difference in R-R intervals within the 3-beat groupings. 
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• BOTTOM LINE: Despite this slightly atypical feature in the two 3-beat groupings — I feel this laddergram confirms that the most likely diagnosis for this rhythm is sinus with 2nd-Degree AV Block, Mobitz Type I ( = AV Wenckebach), in which there is 4:3 AV conduction ( = 4 P waves, of which only 3 are conducted for beats #3,4,5; and #10,11,12) — and — 3:2 AV conduction ( = 3 P waves, of which only 2 are conducted for beats #1-2; #6-7; and #8-9).
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• Correction: My THANKS to Wai Shein — for his "eagle eye" in catching the error in my original description of Figure-6 — which I have now corrected = May 9, 2024).

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ADDENDUM: For those wanting to see the stepwise approach used to arrive at the laddergram I showed in Figure-6 — I’ve added Figures #7-thru-13.

• CLICK on Figure #7 — which will magnify this Figure for you. Then advance one-by-one the next 6 Figures in the magnified mode to see our stepwise approach for drawing this laddergram.

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Figure-7: Laddergram STEP-1. We find it easiest to first complete the Atrial Tier, that shows atrial activity.

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Figure-8: Laddergram STEP-2. We next fill in the Ventricular Tier, to show QRS complexes that we are sure about.

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Figure-9: Laddergram STEP-3. We connected the P wave from the Atrial Tier for beat #1 — to the QRS complex that it conducts to.

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Figure-10: Laddergram STEP-4. We've now filled in all of the sinus-conducted beats (ie, those beats that we are certain about = the first beat in each group).

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Figure-11: Laddergram STEP-5. It should now be easy to see that conduction of the 2nd P wave in each grouping takes a little bit longer ( = the principal characteristic of Wenckebach conduction).

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Figure-12: Laddergram STEP-6. We've now added conduction properties for the 3rd QRS complex in the 2 3-beat groups. Use of a laddergram facilitates seeing that the PR interval preceding beats #5 and 12 is atypical for AV Wenckebach, in that it is not longer than the PR interval preceding beats #4 and 11.

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Figure-13: Finished Laddergram (STEP-7). We complete the laddergram by adding a terminal "butt" to those P waves that are not conducted. 

CONCLUSION: My proposed laddergram shows the rhythm to be sinus with 2nd-Degree AV Block, Mobitz Type I ( = AV Wenckebach) — in which there is 4:3 and 3:2 AV conduction.

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Acknowledgment: My THANKS to Thant Sin Win (from Myanmar) for allowing me to use this tracing and clinical case.

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