Tuesday, November 24, 2020

A Fall and a Rhythm to Recognize



MY Comment by KEN GRAUER, MD (11/24/2020):


The 12-lead ECG and accompanying long-lead rhythm strip shown in Figure-1 — was obtained from an elderly man who experienced a minor fall without serious injury. The patient had no cardiac symptoms — and this ECG was recorded as part of a “thorough assessment”. The patient was on long-term Digoxin — but other than this, no additional information about this case was available.

  • NOTE: Although both the 12-lead and long-lead rhythm strip are angled (slightly distorted) — the quality of these tracings is adequate for interpretation — and — there are important lessons to be learned from this case!


  • WHAT is the rhythm in Figure-1?
  • From a clinical perspective — WHAT does this rhythm tell you until you prove otherwise?

Figure-1: 12-lead ECG and accompanying long-lead rhythm strip from an elderly man who fell — but who had no symptoms at the time these tracings were recorded (See text).

MY Thoughts regarding Figure-1: The rhythm is complex — and I’ll discuss it step-by-step below. What can be said at a glance — is that the rhythm is supraventricular (ie, the QRS is narrow everywhere) — and — that the rhythm is not regular, and not overly fast.

  • Looking at the rest of the 12-lead ECG — the axis is horizontal (about 0 degrees) — there is probable LVH (deep S ~19-20 mm in V2 and cut off S wave after 15 mm in lead V3). The T waves in leads V2-thru-V4 are peaked — although my sense is that given deep anterior S waves and an asymptomatic elderly patient — that this may reflect LV “strain” (that sometimes appears as ST-T wave peaking in anterior leads with LVH). ST-T waves in other leads are not “normal” (ie, some ST-T “scooping” in leads I, V5,V6 — and some ST segment flattening in several limb leads) — but my sense is that there probably are no acute ST-T wave changes in this elderly patient without any chest pain.
  • The interesting component in Figure-1 is the rhythm, which we see best in the long-lead rhythm strip ...


  • Did YOU see evidence of atrial activity in Figure-1?
  • HINT: WHY did I reach for my calipers to answer this question?

ANSWER: In general — the BEST lead to look for atrial activity in is lead II. We define sinus rhythm by the presence of an upright P wave in lead II that is conducting. That said — it’s important to remember that the 2nd-best lead to see atrial activity in is lead V1.

  • I do not see P waves in lead II of the 12-lead tracing in Figure-1. I also do not see P waves in 9 of the other leads. But we definitely do see evidence of regular atrial activity in lead V1 (RED arrows in Figure-2).
  • Calipers allow us to instantly prove that the multiple small-amplitude deflections in lead V1 are truly P waves— because: i) Calipers show these deflections are perfectly regular; andii) We see similarly-timed regular deflections in lead V2 in the 12-lead tracing.
  • Note that regular atrial deflections are seen throughout the long-lead V2 rhythm strip (RED arrows in Figure-2). Some of these deflections are more subtle than others (sometimes being partially hidden within various parts of the T wave) — but using calipers allows us to “walk out” regular P waves throughout the entire long-lead rhythm strip!
  • To further assess this rhythm — it’s important to determine the atrial rate. As I’ve illustrated in a number of prior posts in Dr. Smith’s ECG Blog — this is easy to do using the Every-other-Beat Method (See My Comment at the bottom of the page of the April 15, 2020 post). Vertical YELLOW lines in lead V1 of Figure-2 show the starting and stopping point in the interval measuring the amount of time needed to record 2 P waves. It takes just over 3 large boxes (YELLOW numbers) to record 2 P waves (RED numbers) in Figure-2. Therefore — HALF of the atrial rate is a little slower than 300/3 = about 95/minute. This means that the atrial rate is ~95 X 2 = about 190/minute.
  • PEARL #1: A regular atrial rate of ~190/minute is too fast to be sinus tachycardia. The differential diagnosis is between AFlutter vs ATach (Atrial Tachycardia). The isoelectric baseline between P waves (instead of a “sawtooth” patternand an atrial rate well below 300/minute combine to strongly favor ATach as the underlying atrial arrhythmia.

Figure-2: I’ve labeled the P waves in ECG #1 (RED arrows). I also illustrate the every-other-beat Method for determining the atrial rate (See text).


  • WHY is the rhythm in the long-lead rhythm strip in Figure-2 irregular?
  • HINT: Is there a PATTERN to this rhythm? (ie, Are there any elements that repeat?).

ANSWER: As I said at the outset — this rhythm is complex. Nevertheless — certain points can be made about what we see in the long-lead V2 rhythm strip:

  • There is the suggestion of group beating. By this I mean that there are elements of this rhythm that repeat. For example — the 3 short “pauses” that we see (ie, between beats #1-2; between #6-7; and between #8-9) are all about the same duration — and the PR interval for the P wave that appears before the 1st QRS complex at the end of each pause is equal (ie, the PR intervals before beats #2, 7 and 9 is the same!).
  • Virtually all of the other R-R intervals on this long-lead rhythm strip are of very similar duration (if not, the same duration)!
  • The PR intervals preceding beats #3, 4, 5; 8; 10, 11, 12 all look to be the same.
  • The PR interval preceding beat #6 — is the same as the PR interval preceding beat #13 (albeit these 2 PR intervals are a little bit longer than the PR intervals preceding beats #3,4,5,8,10,11,12).
  • CONCLUSION: The above bullets point out too many findings to be by chance. Therefore, these consistent relationships that are highly unlikely to be by chance tell us — there must be some type of conduction going on in this irregular, long-lead rhythm strip.

PEARL #2: It is sometimes very helpful to “step back” a little bit from the tracing — to gain an overall perspective of the pattern of a complex rhythm. PROVE THIS to yourself. Go BACK to my unlabeled Figure-1— and take another look at the long-lead rhythm strip. Realizing that there is some distortion from the angling in this picture — Isn’t it now easier to appreciate the relationships I highlighted in the bullets of my previous section?

  • Becoming comfortable recognizing group beating and other patterns of beats that repeat — provides an invaluable initial clue that can tell you within seconds that there is some type of conduction.

PEARL #3: It is very common to see Wenckebach conduction in association with both AFlutter and ATach. In today’s case — it was the combination of group beating + multiple PR and R-R intervals that are the same that strongly suggested to me that there was Wenckebach conduction, in this case out of the AV node.

  • An important “Take-Home” point from today’s case — is that even without working out a specific mechanism for how such conduction is occurring — we should strongly suspect that the rhythm is ATach with AV Block (in this case with some type of Wenckebach conduction out of the AV node).

PEARL #4: We were told at the beginning of today’s case that this elderly man has been on long-term Digoxin.

  • The combination of Atrial Tachycardia with Wenckebach Block in a patient taking Digoxin has to strongly suggest Digoxin Toxicity until you prove otherwise!

A Few Words on Digoxin:

Digoxin is not used nearly as commonly as it had been in the past. During my training and early practice years — it seemed like a majority of patients with heart failure and/or atrial fibrillation were on this drug. No longer. That said — selected indications for Digoxin remain — and emergency providers will still encounter a certain number of patients taking the drug. This is important — because Digoxin Toxicity may predispose patients to any of a number of potentially life-threatening arrhythmias.

  • Always inquire what medications the patient in front of you is taking. This is especially important if Digoxin is among the medications your patient is taking — because there is a narrow “therapeutic window” between beneficial vs toxic effects of Digoxin. And, if your patient is on Digoxin — be sure to ask if they may have missed any doses — or if they instead might have taken some “extra doses” of their “heart medication" because they weren’t doing so well. You’ll sometimes be surprised by the answers you receive.
  • For those of us who trained in years past — Digoxin taught many of us more about cardiac arrhythmias than any other factor. This is because Dig excess may cause virtually any arrhythmia (except rapid AFib). Certain rhythms are especially suggestive of Dig toxicity = frequent and/or multiform PVCs; VT; ATach (atrial tachycardia) with block; accelerated junctional rhythm; rhythms with Wenckebach block; very slow AFib. Other rhythm disturbances that may be seen include marked bradycardia, PR interval prolongation, and sometimes complete AV block.
  • A wide range of trough serum Digoxin levels has been cited as “therapeutic”. In years past, this range had been ~0.8-to-2.0 ng/ml — but lower ranges (ie, keeping the trough level ≤1.2 ng/ml — if not below 0.8 ng/ml) are now more commonly recommended. KEY Point: There is a wide “overlap range” between serum Digoxin levels that fall within the “therapeutic range” — and serum Digoxin levels that may precipitate serious Dig toxicity arrhythmias. Acutely ill patients, especially those with renal impairment and/or serum electrolyte disorders (low serum K+ or Mg++) — are especially vulnerable to developing Dig toxic arrhythmias despite serum Digoxin levels that fall within the therapeutic range.

NOTE: All of the above is relevant to today’s case. Unfortunately, we don’t have follow-up for this patient — but given that today’s patient was on long-term Digoxin and presented with ATach + Wenckebach block — we need to strongly suspect Dig Toxicity until proven otherwise (even if the serum Digoxin level were to fall within the “therapeutic” range).

  • P.S.: Much has been made about looking for “Dig effect” on ECG. The literature describes ST segment “scooping” with a relatively short QT interval as the ST-T wave response to high serum levels of this drug. This picture is seen for the ST-T wave in leads V5 and V6 of ECG #1 — but it is not seen in other leads on this tracing.
  • Having worked as full-time faculty for 30 years in an ambulatory primary care center in which we worked closely with our pharmacology colleagues — I had extensive experience interpreting numerous ECGs on patients whose serum Digoxin levels were carefully monitored over time. Doing so taught me the following: iPatients on long-term Digoxin may manifest ST “scooping” in at least several leads (as is seen in leads V5 and V6 of ECG #1) — but not all patients taking Digoxin show such ST-T wave changes; andii) Despite what the literature says — there is no reliable correlation between how high the serum Digoxin level is and the presence or absence of “Dig effect” on ECG. Patients can be Dig toxic despite having normal ST-T waves.

MORE on the Rhythm:

As I noted from the outset — the mechanism of the rhythm in the long-lead rhythm strip is complex.

  • Recognition of Atrial Tachycardia with group beating and the similar R-R and PR interval relationships that I detailed earlier is sufficient to strongly suggest there is Wenckebach conduction (and Wenckebach block) out of one or more levels in the AV node.
  • I propose the Laddergram I show in Figure-3 as the mechanism operative in this case. The laddergram suggests there is dual-level Wenckebach conduction out of the AV node (2:1 and 3:2 conduction at the upper level — with longer Wenckebach cycles in the lower level).
  • Other proposed mechanisms from any of our readers are welcome!

Figure-3: My proposed laddergram for the rhythm in today’s case (See text).


  • NOTE: My sincere THANKS to Edward Brunacci (Australia) for sharing the tracings and this case with us!


ADDENDUM (11/25/2020):
As I've indicated in previous posts in which I have proposed laddergram solutions — there can often be more than a single possible explanation for a given complex arrhythmia. I therefore wanted to publish David Richley's proposed alternative laddergram to the one I show above in Figure-3:
  • Dave writes: I offer an alternative laddergram which proposes that there are long Wenckebach sequences in the upper AV node and 2:1 block at the lower AV node (See Figure-4).
  • Dave adds: I don't know if my proposed alternative laddergram is more or less likely to be true than your explanation, Ken — and I merely offer it as an alternative for consideration!
  • BOTTOM Line: I also don't know if Dave's proposed laddergram is more or less likely than mine — but regardless — the KEY points to this case are unchanged = this elderly patient who is on long-term Digoxin manifests with ATach + some form of multi-AV-nodal level Wenckebach block — and should therefore be considered to have Dig Toxicity until proven otherwise.

Figure-4: David Richley's proposed alternative laddergram (See text).


  1. Ken...

    This is one of my favorite types of dysrhythmias. While I totally agree with your diagnosis, it's your artwork that I have thoughts about.

    First, a few comments for the other readers. For a long time, we thought that multi-level AV blocks (aka "alternate Wenckebach") were very rare. But now we know they aren't. I see them frequently in rhythm strips that get posted on various ECG sites. However, they do not last very long. The block may only last for one or two episodes or the block ratios may change very dynamically from one ratio to another involving one or both levels - which I feel has happened in this ECG.

    And, Ken, though I may disagree with your diagram (which is really a very minor point) your diagnosis of a 2:1 AV block at one level and a Mobitz 1 block in the other level is spot on!

    OK, here's the issue of the diagram which, quite frankly had me very puzzled until I reconstructed the laddergram. You have diagrammed the dysrhythmia as a "Type A" multi-level AV block with the integral ratio (2:1 block) in the upper level and the non-integral ratio (Wenckebach) in the lower level. However, that only gives us two non-conducted P waves at the end of the Wenckebach episode - which does not happen with a Type A multi-level AV block. A Type A block will always have three non-conducted beats at the end of the episode. Now, if you switch the levels, putting the Wenckebach rhythm in the upper level and the 2:1 block in the lower level, you will have a Type B multi-level AV block which can have one, two or even three non-conducted P waves at the end of the Wenckebach episode. Your diagnosis is absolutely correct, but the laddergram is just off a bit.

    If you look at the 12-lead ECG accompanying this rhythm strip, Leads V1 and V2, you will see a true Type A multi-level AV block with three non-conducted P waves at the end of the Wenckebach episode. The ratios were apparently changing even as these tracings were being recorded - which would not be unexpected but could certainly add more confusion to an already confusing dysrhythmia.

    Thanks so much for this post!

    Jerry W. Jones, MD FACEP FAAEM

    1. THANKS so much for your Comment Jerry !!! You have made me go back one more time (about the 20th time I’ve looked at this case) — and I see exactly what you are talking about! There ARE 3 successive non-conducted beats in lead V1 — but NOT in the long lead V2 rhythm strip that was done at a slightly different time — so the ratio of conduction DID indeed change! And you’ll note that since I first published this post — that I added an Addendum with contribution from David Richley — in which he reversed the sequence of the type of block within the AV node. If I understand you correctly — you are simply saying that Dave’s laddergram is likely to be the more accurate one! THANKS again so much for your comment. GREAT discussion! — :)

  2. On the 12 lead in the V1-V3 section I see three none conducted P-waves in a row. When I saw this I thought second degree AV type 2 high grade. But the PR lengthens consistent with wenchebach. To me in the past, multiple dropped beats in a row eliminated wenkebach, but now in the context of toxicity it appears most correct.

    1. Thanks for your comment — which illustrates why it is so important to always have a long lead rhythm strip! This is a complex arrhythmia! With AFlutter and/or ATach — when you have group beating, there is almost always Wenckebach conduction out of the AV node. And when the group vary, and you see more than a single non-conducted P wave in a row — there is usually some form of “multi-level” Wenckebach conduction (even when the patient is not Dig toxic!). Please be sure to look at the Addendum I recently added, in which David Richley reverses the sequence of the type of block within the AV Nodal Tier (See Figure-4 above) — and also the Comment by Jerry Jones (just above yours) that explains this further …. So YES — multiple dropped beats in a row CAN be due to Wenckebach block (and the mechanisms can get quite complicated and involve multiple levels within the AV Node!) — :)

  3. Dear Mr. Grauer! Thank you so much for so unwavering investment in explaining the intricate art of reading ECGs.

    I have a question about the laddergram of your post on 11/24/2020.
    When there are two p waves that do not conduct preceding one that does, you drew the conduction of the first of the non-conducting ones longer (passing over the middle line of the AV node) than the second one (stopping before the midline).
    Why did you do that?

    Thank you very much again!

    All the best, stay negative (ly Covid)!

    Mario from Germany

    1. Hi Mario. THANK YOU for your comment. As I just now answered to the question by “b-climb” — this is a complex arrhythmia! With AFlutter and/or ATach — when you have group beating, there is almost always Wenckebach conduction out of the AV node. And when the groups vary, and you see more than a single non-conducted P wave in a row — there is usually some form of “multi-level” Wenckebach conduction (even when the patient is not Dig toxic!).

      So — I fully acknowledge that I did not know the precise mechanism of this rhythm before I sat down to draw the laddergram (although I knew that there was ATach with some form of dual level Wenckebach conduction out of the AV node). And as I always do with laddergrams — I first contruct the Atrial Tier ( = P waves) — then I construct the Ventricular Tier ( = the QRS complexes) — and I always save the AV Nodal Tier for LAST! I played around with a couple of possibilities until I came up with the one that I thought was most logical (which I show in Figure-3). But please note in my Addendum, that David Richley (who is extremely astute in uncovering the mechanism of complex arrhythmias) came up with a slightly different approach when he completed the AV Nodal Tier in his laddergram (See Figure-4).

      MOST of the time (ie, well over 90-95% of all of the laddergrams that I draw) — I find there is only a single explanation that I usually know BEFORE I finish my laddergram (in which case the reason why I draw such laddergrams is to illustrate the mechanism to others). But on occasion (as in this tracing) — I needed the laddergram to help ME come up with a logical mechanism. And as can be seen from David Richley’s proposal — mine is not the only possible explanations for the mechanism of this complex arrhythmia. I hope the above provides insight to you! — :)


DEAR READER: I have loved receiving your comments, but I am no longer able to moderate them. Since the vast majority are SPAM, I need to moderate them all. Therefore, comments will rarely be published any more. So Sorry.

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