Thursday, May 19, 2022

ECG Blog #306 — Alternating Beats

The ECG in Figure-1 — was obtained from a 60-year old woman, who presented to the ED (Emergency Department) with intermittent shortness of breath over the past week. No chest pain. The patient has a history of diabetes and hypertension.
  • How would YOU interpret the ECG in Figure-1?
  • Why are there "alternating" beats?

Figure-1: 12-lead ECG obtained from a 60-year old woman with intermittent dyspnea (but no chest pain).

NOTE: Today’s tracing is another ECG “Quick Case” ( EQC) — in that I’ll provide a more “time-efficient” account of my thought process (with goal toward expediting your interpretation within seconds rather than minutes)! Relevant links are at the bottom of the page.


MY Thoughts on the ECG in Figure-1:
The technique for recording today's ECG provides us with a continuous look at the rhythm — but the leads switch halfway through.
  • The advantage of this technique — is that it provides us with a simultaneous look at the first 9 beats in each of the 6 limb leads — and then, a simultaneous look at beats #10-thru-17 in each of the 6 chest leads.
  • The disadvantage — is that we do not get to see the rhythm strip recorded entirely from the perspective of any one lead.

Even before applying the Ps, Qs, 3R Approach for assessing the rhythm (as described in ECG Blog #185) — I was "struck" by the picture of "alternating" beats in Figure-1. By this I mean — that the shape of each QRST complex changes every-other beat. In this sense — this is a bigeminal rhythm.
  • I reviewed the concept of "Bigeminy" — and the common bigeminal rhythms in ECG Blog #243. Given the obvious widening of every-other-beat in Figure-1 — the principal diagnostic considerations would be distinction between: i) Ventricular bigeminy (in which every-other-beat is a PVC); ii) Atrial or junctional  bigeminy (in which every-other-beat is a PAC or PJC — with QRS widening resulting from either preexisting bundle branch block or aberrant conduction)vsiii) Sinus rhythm with a conduction defect such as bundle branch block occurring every-other-beat.

PEARL #1: As is so often the case — the simple act of labeling all P waves is often revealing (Figure-2).
  • RED arrows in Figure-2 show that the underlying rhythm is a regular sinus tachycardia at ~120/minute. Doesn't the PR interval look to be the same in front of each of the 17 beats on today's tracing?

PEARL #2: If the reason for the alternating beats in Figure-2 is atrial, junctional or ventricular bigeminy — then the wider beats should be "premature" (ie, PACs, PJCs and PVCs are all characterized by their early occurrence before the next expected sinus beat).
  • Therefore — the KEY to diagnosing the etiology of the rhythm in Figure-2, is to carefully measure the R-R interval from the beginning of a normally-conducted sinus beat — until the beginning of a wider sinus-conducted beat ( = the R-R interval marked "A" in both limb leads and chest leads).
  • Then compare this interval "A" — to the R-R interval marked "B", which extends from the onset of a wider sinus-conducted beat — until the next normally-conducted (narrower) beat.
  • In both limb leads and chest leads — interval "A" is precisely equal to interval "B". And since the PR interval preceding all beats in this tracing is the same — this confirms that all beats in Figure-2 are sinus-conducted with the same PR interval. The only thing changing — is that the QRS complex becomes wider every-other-beat — because all even-numbered beats in Figure-2 ( = beats #2,4,6,8,10,12,14,16) are being conducted with LBBB (Left Bundle Branch Block)

Figure-2: I have labeled all P waves from Figure-1 — and compare the R-R intervals of alternating beats (See text).

Intermittent Bundle Branch Block:
We are used to seeing conduction defects (ie, RBBB, LBBB, IVCD, hemiblocks) occur with every beat. On occasion — conduction defects may be "rate-related" (usually in association with an increase in rate — in which the QRS widens when the rate accelerates to a certain amount — and then narrows again after the rate slows down).
  • Conduction defects can also be intermittent. Usually this occurs with a "fixed" interval of time between beats that conduct normally, and wider beats that manifest the conduction defect (ie, most often showing the intermittent conduction defect  every 2nd, every 3rd, or every 4th beat). This is the situation with today's tracing — in which we see LBBB conduction every-other-beat.
  • On occasion — the intermittent conduction defect may show random alternation between normal and impaired conduction, with no "fixed" interval between narrow and wider beats (See My Comment in the June 25, 2020 post in Dr. Smith's ECG Blog).

What We Can Learn from Intermittent BBB Conduction!
Because conduction defects alter the sequence of ventricular depolarization — the sequence of ventricular repolarization will also be changed! As a result — it will always be more challenging to evaluate ST-T wave changes in association with a conduction defect (especially with LBBB — which alters the initial vector of ventricular depolarization).
  • PEARL #3: Today's tracing offers the unique opportunity to see the effect that LBBB may have in each of the 12 leads of an ECG. To facilitate visualizing this effect — I first color in BLUE the odd-numbered beats which are conducted normally (Figure-3). Doing so allows us to appreciate the even-numbered beats — which are conducted with LBBB.

  • NOTE: QRS morphology for the even-numbered beats in Figure-3 is typical for LBBB in the limb leads (ie, monophasic, all upright R wave in high-lateral leads I and aVL). The straight descent with predominant negativity for the anterior leads is typical for LBBB — although lead V6 lacks the monophasic R wave usually expected with typical LBBB.

  • PEARL #4: With LBBB — the finding of very deep S waves in one or more of the anterior leads (ie, deeper than 25-30 mm) suggests LVH. This is seen is leads V1 and V2 (which manifest S waves of 30 and 25 mm, respectively).
  • Because the left ventricle enlarges not only to the left, but also posteriorly with LVH — some patients with LBBB will not manifest an all-upright R wave until we arrive at a lead more lateral than lead V6 (ie, a lead V7 or V8). However, given how typical the morphology of even-numbered beats is for LBBB in both high-lateral and anterior leads — I'd assess the conduction defect in this tracing consistent with LBBB.

  • As discussed in ECG Blog #204 and ECG Blog #282 — ST-T waves for the even-numbered beats in Figure-3 that are conducted with LBBB morphology do not suggest acute infarction.

Figure-3: I've colored in BLUE the odd-numbered beats that manifest normal conduction. This facilitates assessment of the even-numbered beats — which manifest LBBB conduction (See text).

PEARL #5: Assessment of acute ST-T wave changes is best made by identifying the normally-conducted sinus beats in a tracing. To facilitate this assessment — I've colored in YELLOW the even-numbered beats in Figure-4, which are conducted with LBBB.
  • While true that it will at times be possible to identify acute ST-T wave changes in beats conducted with bundle branch block — I always begin by focusing on ST-T wave assessment of normally conducted beats, as it's usually much easier to spot abnormal findings in sinus-conducted beats.

  • Note in Figure-4 — that there is diffuse ST depression (ie, in almost all leads — most marked in leads V3-thru-V6) in the normally-conducted beats. This occurs in association with ST elevation in these odd-numbered beats in lead aVR.

PEARL #6: Recognition of the ECG pattern seen in Figure-4 for the normally-conducted beats — in which there is diffuse ST segment depression (usually present in at least 7-8 leads+ ST elevation in lead aVR — should immediately suggest the following Differential Diagnosis:
  • Severe Coronary Disease (due to LMain, proximal LAD, and/or severe 2- or 3-vessel disease) — which in the right clinical context may indicate ACS (Acute Coronary Syndrome).
  • Subendocardial Ischemia from another Cause (ie, sustained tachyarrhythmia; cardiac arrest; shock/profound hypotension; hypoxemia; GI bleeding; anemia; "sick patient"; etc.).
To EMPHASIZE: This pattern of diffuse Subendocardial Ischemia does not suggest acute coronary occlusion (ie, it is not the pattern of an acute MI) — but rather ischemia due to the above differential diagnosis!

Figure-4: I've colored in YeLLOW the even-numbered beats that manifest LBBB conduction. This facilitates assessment of the odd-numbered beats — which are normally conducted (See text).

FINAL Comparison:
I complete my discussion of this deceptive rhythm — by isolating in Figure-5, a direct comparison between normally-conducted beats vs beats conducted with LBBB:
  • I find it insightful to directly compare QRS and ST-T wave morphology of the normally-conducted sinus beats (ie, beats #3 and 11)vs — beats conducted with LBBB (ie, beats #4 and 12).

Figure-5: Direct comparison between normally-conducted beats vs beats conducted with LBBB.

Putting It All Together:
Today's tracing was obtained from a 60-year old woman, who presented to the ED with intermittent dyspnea (but no chest pain) over the past week. The patient had a history of diabetes and longstanding hypertension.
  • The rhythm in today's tracing is sinus tachycardia at ~120/minute. Every-other-beat is conducted with LBBB. The very deep anterior S waves in beats conducted with LBBB suggests LVH. The marked and diffuse ST depression, with ST elevation in lead aVR — suggests diffuse subendocardial ischemia.
  • As suggested above in Pearl #6 — diffuse subendocardial ischemia could be due to severe coronary diseaseor — to some other cause. The patient's age, co-morbidities (ie, diabetes, hypertension) and symptoms (dyspnea, albeit without chest pain) — clearly predispose to coronary disease. IF there is no heart failure or other potentially treatable disorder — cardiac cath may be needed to clarify the anatomy. 

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

Relevant ECG Blog Posts to Today’s Post: 

  • See ECG Blog #185 — for review of the Systematic Ps, Qs, 3R Approach to Rhythm Interpretation.
  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.

  • ECG Blog #204 — Reviews a user-friendly approach to the ECG Diagnosis of conduction defects (ie, LBBB — RBBB — IVCD).

  • ECG Blog #282 — Reviews application of modified-Smith-Sgarbossa Criteria for evaluation acute MI with LBBB (as well as ECG diagnosis of LVH with LBBB).

  • ECG Blog #271 — Reviews the ECG diagnosis of diffuse subendocardial ischemia.

  • ECG Blog #198 — An Irregular WCT (LBBB or IVCD).
  • ECG Blog #162 — LBBB with obvious STEMI.
  • ECG Blog #146 — LBBB with Acute ST-T Wave Changes.
  • ECG Blog #204 — Assessment of Sinus Rhythm and a Wide QRS (due to IVCD).

  • The January 31, 2022 post in Dr. Smith's ECG Blog — Reviews subtle signs of acute OMI in a patient with LBBB (Please see My Comment at the bottom of the page).
  • The June 25, 2020 post in Dr. Smith’s ECG Blog — in which I review a case of Sinus Rhythm with Intermittent RBBB.

Sunday, May 15, 2022

ECG Blog #305 — The Cause of Palpitations?

The ECG and long lead II rhythm strip in Figure-1 — was obtained from a previously healthy middle-aged woman, with a history of intermittent palpitations over the past few months. No syncope or chest pain. She was hemodynamically stable at the time this ECG was recorded.

  • How would YOU interpret the ECG in Figure-1?
  • What might cause this rhythm?

Figure-1: 12-lead ECG and long lead II rhythm strip recorded on a middle-aged woman with palpitations in recent months. Hemodynamically stable.

MY Thoughts on the ECG in Figure-1:
As always — I favor starting by assessing the cardiac rhythm. Applying the Ps, Qs, 3R Approach (ECG Blog #185) — to the long lead II rhythm strip at the bottom of the tracing:

  • The QRS is narrow everywhere (which we can confirm by verifying that every beat in the 12 leads above the rhythm strip has a narrow QRS).
  • The rhythm is fast and irregularly irregular. But unlike Atrial Fibrillation (AFib) — there are P waves! (Figure-2).

PEARL #1: It is sometimes difficult to distinguish between baseline artifact vs different-shaped P waves. And, sometimes both artifact and different shaped P waves (PACs) may be present:

  • This is not the case in today’s tracing! There is essentially no artifact in the baseline or within ST-T waves. As a result — What we see on this tracing is valid!
  • There is NO doubt that an upright P wave with reasonable PR interval precedes each QRS complex that follows a short pause (ie, BLUE arrows before beats #2, 6, 7, 12, 16 and 17 in Figure-2).

  • PEARL #2: The P wave in front of beat #2 in the long lead II rhythm strip deserves special mention — because it is tiny. This is the benefit of assessing the rhythm by use of simultaneously-recorded leads! A quick look straight above beat #2, at the 2nd BLUE arrows in lead I and in lead III (vertical RED lines that correspond in timing to the P wave in front of beat #2 in the long lead rhythm strip)confirms that there is a P wave in front of beat #2 in the long lead rhythm strip, albeit a P wave that looks different (smaller) than all other P waves in this long lead II (except for the equally tiny P wave in front of beat #1).

  • PEARL #3: I find the most helpful way to determine when and where P waves might be hiding (within their preceding ST-T wave) — is to figure out WHAT a “normal” ST-T wave looks like. In Figure-2 — I thought the ST-T wave of beats #1, 11 and 15 represent what a “normal” ST-T wave (ie, not altered by a PAC hidden within it) should look like. 

  • PEARL #4: The commonest cause of a pause is a blocked PAC! (See ECG Blog #14 and Blog #66). Awareness of this clinical reality has led me to always look carefully at the ST-T wave at the beginning of any relative pause in the rhythm — to see if there might be a P wave partially "buried" within that ST-T wave. And so, I thought the YELLOW arrows that occurred right after beats #6 and 16 clearly represented non-conducted atrial activity — with the notching under these arrows highlighting blocked PACs.

My Initial Impression of the Rhythm in Figure-2:
Having established that the rhythm in Figure-2 was supraventricular (narrow QRS) — and both fast and irregular — but not AFib because there clearly was atrial activity — I contemplated my differential diagnosis:
  • P wave morphology was not consistent. For example — the tiny P waves in front of beats #1 and 2 in the long lead II rhythm strip clearly looked different than the larger and rounder P waves that precede beats #7, 16 and 17. And the P wave in front of beat #12 looked taller still, as well as being more pointed. Therefore — my initial impression of this rhythm was MAT (Multifocal Atrial Tachycardia).

And then I looked again more carefully ...

Figure-2: I've labeled atrial activity from Figure-1 with BLUE arrows. I've labeled non-conducted P waves with YELLOW arrows. The vertical RED lines illustrate PEARL #2, which describes use of simultaneously-recorded leads (See text).

Regarding MAT: What Does Not "Fit" for Today's Patient:
I have previously reviewed the ECG diagnosis of MAT (See ECG Blog #199 and Blog #65).
  • MAT almost always occurs in one of 2 common predisposing settings. These 2 settings are: i) In patients with severe, often longstanding pulmonary disease; and/or, ii) In acute ill patients with multi-system disease (ie, sepsis, shock, electrolyte and/or acid base disorders). As a result — I'm hesitant to diagnose MAT in the absence of one of these 2 settings. The fact that today's patient was a previously healthy middle-aged woman is therefore against the likelihood of seeing MAT.

While labeling today's ECG for Figure-2I looked again at the long lead II rhythm strip. In Figure-3 — I've added a number of additional YELLOW arrows where the ST-T wave appears to be clearly deformed by additional non-conducting atrial activity. For many of these additional YELLOW arrows — we can see indication of partially hidden atrial activity of other simultaneously-recorded leads.
  • LOOK AGAIN at the long lead II rhythm strip in Figure-3. If you can accept the validity of the colored arrows I've added — after the first 2 P waves in each grouping — Aren't the BLUE and YELLOW arrows that follow until the pause fairly regular?

  • PEARL #5: Not all rhythms "read the textbook". While we often think of entities such as Atrial Tachycardia and MAT as "pure" rhythm etiologies — many patients do not manifest "pure" versions of these arrhythmias. I've found it best to consider entities such as ATach, MAT, wandering atrial pacemaker, and sinus rhythm with multiple PACs as ends of a "spectrum"with many patients manifesting more of a "mixture" between the spectrum end points for these various rhythm disorders.

MY "Revised" Rhythm Diagnosis:
While emphasizing that today's rhythm does not perfectly fit any of the rhythm etiologies that I mention above — I think it is closest to ATach.
  • Remember — The atrial rate with ATach is not always regular. On the contrary — ectopic atrial tachycardia is more likely to manifest a "warm-up" phase until this rhythm gets going. Perhaps the slightly longer P-P intervals at the beginning of each grouping represent such a "warm-up" phase?
  • Even with atrial impulses arising from the same site — P wave morphology may vary. Isn't it strange that the PR interval is the same for so many of the different-looking P waves in Figure-3 (ie, the P waves in front of beats #1, 2, 6, 7, 12, 13, 16 and 17). I would not expect the PR interval to remain the same for so many beats if the underlying rhythm was MAT.

  • ATach (Atrial Tachycardia) very commonly manifests Wenckebach conduction. Therefore, rather than "blocked PACs" — Perhaps the YELLOW arrows that I've drawn in Figure-3 represent non-conducted P waves from short ATach-related Wenckebach cycles?

BOTTOM LINE Regarding Today's Case:
I fully acknowledge that I do not know a definitive answer for the rhythm etiology in today's case. That said — I believe this rhythm is "clinically behaving" like an ectopic ATach in this previously healthy middle-aged woman who has intermittently been bothered by recurrent palpitations over the past few months.
  • In order is a General Evaluation of this patient — to include chest X-Ray, Echo and baseline lab work (ie, thyroid function, serum electrolytes, hematocrit).

  • Verify in this patient's History the duration of her symptoms — and determine IF she is a longterm smoker (that might predispose to MAT) — and/or if there is significant alcohol, drug, caffeine or other substance use that might predispose her to a recurrent irregular SVT.
  • IF these results did not yield clues to the etiology of today's rhythm — then empiric treatment with a medication such as a ß-blocker might be in order.

  • IF her palpitations (and this rhythm) persisted — referral to EP Cardiology would be in order.

Figure-3: The more I looked at this tracing — the more indication I saw of more atrial activity (additional BLUE and YELLOW arrows drawn in since Figure-2).


Acknowledgment: My appreciation to Arjun K Budhathoki (from Kathmandu, Nepal) for making me aware of this case and allowing me to use this tracing.


Relevant ECG Blog Posts to Today's Post:
  • ECG Blog #185 — Reviews the Ps, Qs, 3R Approach to Rhythm Interpretation.

  • ECG Blog #199 — Reviews the ECG diagnosis of MAT (including a Video Pearl on this subject).
  • ECG Blog #65 — Another example of MAT (vs Wandering Pacemaker).

  • ECG Blog #250 — Causes of a Regular SVT (including AFlutter & ATach).
  • ECG Blog #138 — ATach vs AFlutter.
  • ECG Blog #261 — Reviews a case of ATach with Wenckebach conduction.

Wednesday, May 11, 2022

ECG Blog #304 — What Kind of Rhythm?

Today's CASE: 
The 12-lead ECG and long lead I rhythm strip in Figure-1 — was obtained from a 65-year old woman who presented to the ED (Emergency Department) a 1-day history of chest pain. Her chest pain had resolved at the time the ECG in Figure-1 was recorded.


  • How would YOU interpret the rhythm and the 12-lead?
  • What do you think may have happened?

  • Extra Credit: Why is interpretation of this tracing so challenging? HINT: The answer relates to the technical way in which this tracing was recorded.

Figure-1: 12-lead ECG and long lead I rhythm strip from a 65-year old woman with chest pain (See text).

WHY is Interpretation of this Tracing so Challenging?
There are several reasons that contribute to why interpretation of today's tracing is so challenging:
  • Looking first at the long lead I rhythm strip at the bottom of the tracing — Note that QRS morphology changes several times! In order to determine WHY this might be so — we would need to be able to look at a simultaneous recording in other leads. But the fact that not all of the QRS complexes in the long lead I rhythm strip line up vertically (ie, directly under corresponding beats in the 12-lead tracing)negates the possibility of using additional leads to help determine the etiology of all beats in the long lead I.

This concept is best understood by looking at the colored arrows in Figure-2:
  • The technique that was used to record the ECG in today's case was to show the first 5 beats in the tracing twice! To illustrate this — I've numbered the beats #1-thru-5 in the 6 limb leads. These same 6 beats are again shown in the 6 chest leads. 
  • The "advantage" of this technique — is that we get to see what these first 5 beats in today's tracing look like in each of the 12 leads (ie, vertical RED arrows in Figure-2 show that the first 5 beats in the long lead rhythm strip are simultaneously-recorded with the 6 limb leads).
  • That said — the disadvantages of this technique are: i) That we only see what the first 5 beats look like in other leads (ie, we have no idea what beats #6-thru-10 in the long lead I rhythm strip look like in other leads); and, ii) The 2nd part of the long lead rhythm strip is not simultaneously-recorded with the chest leads (vertical BLUE arrows in Figure-2 that do not line up with the 5 QRS complexes in the chest leads).

  • KEY Point: It is because QRS morphology changes several times in the long lead I rhythm strip — that simultaneous recording in other leads is essential for determining the etiology of beats #6, 7 and 10! But since we have no idea what these beats look like in the other chest leads — I simply could not be certain if beat #6 is a fusion beat? — nor if beats #7 and 10 reflect bradycardia-induced aberrant conduction or ventricular escape?

  • PEARL #1: One of the most valuable tools in advanced arrhythmia interpretation of complex tracings is the use of simultaneously-recorded leads — that allow us to assess problematic beats in the long lead rhythm strip compared to their appearance in other leads of the 12-lead tracing. It's important to appreciate how the technique used to record today's tracing deprives us of the use of this tool.

Figure-2: I've labeled which beats in the 12-lead ECG correspond to which beats in the long lead I rhythm strip at the bottom of the tracing. The vertical BLUE arrows show that beats #6-thru-10 in the long lead rhythm strip do not correspond to the 5 beats recorded in the chest leads (See text).

What then is the Rhythm in Today's Tracing?
Realizing that the lack of a simultaneously-recorded long lead rhythm strip prevents accurate assessment of all variations in QRS morphology — there are certain things we can say about the rhythm in today's tracing:
  • Sinus P waves are present! Although small in amplitude — and partially hidden in certain parts of the long lead rhythm strip — use of calipers allowed me to "walk out" regularly-occurring sinus P waves at a rate of ~100/minute (RED arrows in Figure-3).

  • PEARL #2: In a complex tracing such as this one — START by looking at those beats in the rhythm that are easiest to interpret. Save the more difficult parts of the tracing for LAST.
  • Beats #5, 8 and 9 are narrow. These beats are clearly supraventricular.
  • Beat #6 is also narrow — albeit a little bit taller and wider than beats #5,8,9. I suspect beat #6 is also supraventricular, perhaps with either aberrant conduction or partial fusion (ie, to account for its slightly larger size compared to beats #5,8,9).
  • Beats #1, 2, 3 and 4 all manifest the same QRS morphology. The initial narrow R wave (with similar slope and direction for the initial part of the QRS as is seen for beats #5,8,9 in the long lead rhythm strip) — together with their terminal wide S wave — suggests that beats #1,2,3,4 are supraventricular with RBBB conduction.

  • NOTE: The R-R interval is constant for these first 4 beats in Figure-3 (ie, the R-R interval ~6 large boxes, corresponding to a rate of ~50/minute). However, the PR interval continually changes for these first 4 beats — and none of the P waves (RED arrows) have a chance to conduct. This suggests that there is AV dissociation (ie, non-conduction) for the P waves contained within these first 4 beats — with an appropriate junctional "escape" rate of ~50/minute.

  • PEARL #3: One of the BEST clues that AV block is not complete — is when you see a supraventricular complex occur earlier-than-expected! Note that compared to the R-R interval for the first 4 beats in the tracing — beat #5 occurs earlier-than-expected! This strongly suggests that beat #5 is being conducted!

  • Now that we know that beat #5 is being conducted — Note that the PR interval for beat #5 is long! (ie, about 400 msec.). Thus, there is marked 1st-degree AV block for this conducted beat!
  • Also — Since beat #5 is being conducted — the degree of AV block in Figure-3 is not complete (ie, This is not 3rd-degree AV block). But since a number of P waves are clearly not being conducted — the rhythm in Figure-3 must represent some form of 2nd-degree AV block.

NOTE: If you are like me — you have already taken a "peek" at the 12-lead ECG. If so — you've probably noted suggestion of recent (if not acute) inferior MI.
  • PEARL #4: Of the 2nd-degree AV blocks — Mobitz I is far more common than Mobitz II (ie, In my experience — more than 90-95% of all 2nd-degree AV blocks are Mobitz I). And IF (as we see in today's case) — your patient manifests: i) A narrow QRS complex for conducted beats; ii) A long PR interval for conducted beats; and, iii) Evidence of recent or acute inferior infarction — then it is almost certain that the type of 2nd-degree AV block will be Mobitz I ( = AV Wenckebach).

Editorial COMMENT: For time-efficiency — I temporarily interrupted my assessment of the rhythm at this point, in order to look closer at the rest of the 12-lead tracing.
  • I did this because: i) I had already established extremely high likelihood that some type of 2nd-degree Wenckebach was present; and, ii) This tracing is complicated enough that I knew I would need an extra "moment of time" to draw a laddergram if I wanted to more accurately work out the potential mechanism of the arrhythmia.

To EMPHASIZE: You do not need to know the precise mechanism of every arrhythmia you encounter in order to know how to manage the patient. 
  • Simply recognizing that some type of 2nd-degree AV block, which is probably a form of Wenckebach (as per Pearl #4) — is more than enough in today's case to initiate appropriate management.
  • Use of laddergrams is a superb way to illustrate the mechanism of complex arrhythmias. That said — except for exceedingly complex arrhythmias, I only rarely need to draw a laddergram to interpret a rhythm.

  • For those interested — I illustrate step-by-step how to understand (and/or draw) Laddergrams on ECG Blog #188 (including links to over 50 explained examples of clinical laddergrams that I have drawn).

Figure-3: I've labeled regularly-occurring sinus P waves with RED arrows (See text). 

MY Thoughts on the 12-Lead ECG:
Let's return to Figure-3 — with a goal to assess what is going on in the rest of this 12-lead tracing in this 65-year old woman with a 1-day history of chest pain.
  • There are large Q waves, in association with marked ST elevation and deep T wave inversion in leads III and aVF. Less pronounced but similar findings appear to also be present in the 3rd inferior lead ( = lead II) — although marked artifact and small amplitude of the QRST complex in lead II make this lead more difficult to assess.
  • Note the mirror-image opposite shape of the ST-T wave in lead III and lead aVL. The appearance of these 4 limb leads (ie, leads II, III, aVF; and lead aVL)confirms a recent (if not acute) inferior STEMI.

  • Complicating assessment of today's tracing — is RBBB conduction for the first 4 beats (ie, typical triphasic rSR' complex as seen in lead V1 — in association with wide terminal S waves for these 4 beats in lateral leads I and V6).

  • In the Chest Leads — the ST-T wave appearance in lead V2 is the most remarkable finding. Despite RBBB conduction for the first 4 beats (which usually results in some ST-T wave depression) — the T wave in lead V2 is exceedingly tall (ie, >10 mm!) and peaked.
  • Note that this disproportionate T wave appearance is also seen in lead V2 for beat #5, in which th QRS is narrow (Rememberit was beat #5 that we determined above was being conducted with a narrow QRS complex and long PR interval).
  • The T waves in leads V3 (and probably also in V4) are also "hypervoluminous".

  • It appears that this 65-year old woman with a 1-day history of new chest pain has had an infero-postero STEMI — with resultant 2nd-degree AV block manifesting periods of AV dissociation and Wenckebach conduction.
  • Especially in view of the location of her STEMI (ie, inferior) — and the finding that conducted beats (ie, beats #5, 8 and 9 in the long lead I rhythm strip) manifest a narrow QRS complex — the type of 2nd-degree AV block that she has is almost certain to be Mobitz I. As long as her heart rate does not excessively slow (and as long as she remains hemodynamically stable) — she might not necessarily need a pacemaker.
  • Although there remains some residual inferior lead ST elevation — the depth of inferior lead T wave inversion — and the height of T waves in lateral leads I, aVL and especially in lead V2 — strongly suggest evolution of her STEMI following spontaneous reperfusion of her infarction. (Remember that anterior leads V2,V3,V4 manifest a "mirror-image" of what goes on in the posterior wall — such that tall anterior T waves convey similar implication as the deep T wave inversion in the inferior leads = reperfusion T waves!).
  • NOTE: For more on distinction between deWinter T Waves vs Reperfusion T waves from Posterior MI — See ECG Blog #266.

  • The inferior lead Q waves are consistent with inferior wall necrosis.
  • Note that the QRS complex of beat #5 in the chest leads manifests a QS complex in anterior leads V1,V2,V3 — with abrupt transition to an all-positive QRS by lead V4. This suggests that anteroseptal infarction has occurred at some point in time. I suspected this was not the acute problem — because the rest of the tracing (including the rhythm disorder) was much more suggestive of recent occlusion of the RCA (Right Coronary Artery) — and not the LAD (Left Anterior Descending) coronary artery. That said — cardiac damage is cumulative — so these ECG findings are consistent with multi-vessel disease.

  • CASE Follow-Up: The CATH Report — The patient in today's case became bradycardic and hypotensive — so she ultimately did require a pacemaker. Cardiac cath revealed multi-vessel disease with acute occlusion of the RCA as the "culprit" artery. Thus — this cath report was completely consistent with the above suppositions from assessment of her initial ECG!


MORE on the Rhythm in Today's Case:
I'll conclude today's case with my proposed laddergram for the rhythm in Figure-3. As emphasized earlier — lack of a simultaneously-recorded long lead rhythm strip for all 10 beats of today's tracing prevent me from being certain about the etiology of beats #6, 7 and 10.
  • Rosenbaum said, "After all, every self-respecting arrhythmia has at least 3 possible interpretations". It is common in the "world of complex arrhythmias" — for there to be more than a single possible explanation for the mechanism of a complex rhythm. Sometimes, the only way to know for certain what the true mechanism of an arrhythmia is — is in the EP (ElectroPhysiology lab).
  • Therefore — I am not certain that my proposed laddergram in Figure-4 is correct. But I believe it does present a potentially valid explanation for what we see in this tracing.

Figure-4: My proposed laddergram for the rhythm in today's case (See text).

My Laddergram in Figure-4 Explained:
I always begin development of my laddergram by drawing in atrial activity (vertical RED lines in the Atrial Tier — corresponding to the regular atrial rhythm that we were able to "walk out" with calipers).
  • As I deduced earlier — the finding of RBBB conduction for the first 4 beats in this tracing — in association with a regular R-R interval (corresponding to a rate of ~50/minute) — and no relation between P waves and neighboring QRS complexes for these first 4 beats — suggested to me that these first 4 beats represent an appropriate junctional escape rhythm (drawn in BLUE on the laddergram).
  • Beat #5 is early — manifests a narrow QRS complex — and is preceded by a P wave with a long PR interval. As I indicated earlier (ie, in Pearl #3) — the BEST clue that a beat is conducting in a complex AV block tracing — is that this beat occurs earlier-than-expected and is preceded by a P wave.
  • The PR interval preceding narrow beat #8 looks similar to the prolonged PR interval preceding narrow beat #5. This suggested to me that beat #8 is probably also conducting (in similar fashion as is beat #5).
  • Since the 1st beat on this tracing to conduct needed a long PR interval to do so (ie, of ~400 msec.) — I thought it likely that the fairly short PR intervals preceding beats #6 and 9 might be too short to conduct. IF they were — then perhaps the P waves occurring within the ST segments of beats #5 and 8 might be conducting with an even more prolonged PR interval. (NOTE: I call this "thinking outside-of-the-box" — because it is counterintuitive to postulate that P waves with such a long PR interval are conducting — but the P waves with much shorter PR intervals before beats #6 and 9 are not).
  • I can not rule out the possibility that wider beats #7 and 10 might represent ventricular escape — BUT — if we instead postulate bradycardia-induced LBBB aberration — isn't the pattern after beat #4 in my proposed laddergram perfectly consistent with the complex AV Wenckebach type of 2nd-degree AV block that might be expected with acute inferior infarction?

  • P.S. Feel free to Write Me if you believe you have a more logical explanation for the mechanism for today's rhythm!
  • P.P.S. Regardless of whether or not the arrhythmia mechanism I propose is completely accurate — there is some form of 2nd-degree AV block that almost certainly involves Wenckebach conduction — so clinical (and treatment) implications of my interpretation will be valid!


Acknowledgment: My appreciation to Narong Roth (from Batdambang, Cambodia) for making me aware of this case and allowing me to use this tracing.


Relevant ECG Blog Posts to Today's Post:
  • ECG Blog #204 — Reviews the ECG diagnosis of BBB (reviewed in the Video Pearl).
  • ECG Blog #203 — Reviews a user-friendly approach to the Hemiblocks and to Bifascicular Block.

  • ECG Blog #236 — Reviews the 3 types of 2nd-Degree AV Block.
  • ECG Blog #192 — Reviews the 3 causes of AV Dissociation.

  • ECG Blog #221 — How to diagnose acute MI when there is RBBB (reviewed in the Audio Pearl).
  • ECG Blog #298 — Reviews a case of RBBB/LAHB + Post. MI.

  • ECG Blog #188 — Reviews all about Laddergrams!

  • ECG Blog #185 — Use of a Systematic Approach to Rhythm Interpretation. 
  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
  • ECG Blog #246 — Review use of the "Mirror Test" for the diagnosis of acute posterior MI.
  • ECG Blog #258 — Reviews HOW to "Date" an Infarction. 
  • ECG Blog #184 — Reviews the "magical" mirror-image opposite relationship with acute ischemia between lead III and lead aVL.

  • ECG Blog #262Acute inferior MI + AV Wenckebach
  • ECG Blog #55 — Acute inferior MI + AV Wenckebach. 
  • ECG Blog #154 — Acute inferior MI + AV Wenckebach. 
  • ECG Blog #168 — Acute inferior MI + Wenckebach (dual-level) block. 
  • ECG Blog #224 — Acute inferior MI + AV Wenckebach.
  • ECG Blog #188 — How to Read (and DrawLaddergrams. 

Saturday, May 7, 2022

ECG Blog #303 (EQC) — The Patient Fainted

Today’s tracing is another ECG “Quick Case” ( = EQC) — in which I’ll provide a more “time-efficient” account of my thought process (with goal toward expediting your interpretation within seconds rather than minutes)! Relevant links are at the bottom of the page.


Today's CASE: 
The 12-lead ECG and long lead II rhythm strip in Figure-1 — was obtained from an older woman who “suddenly fainted”. No chest pain.


  • How would YOU interpret the rhythm and the 12-lead?
  • What do you think may have happened?

Figure-1: ECG from an older woman who fainted. No chest pain.

MY Thoughts on the Initial ECG in Figure-1:

The rhythm is regular at ~50-55/minute. The QRS is wide. Looking at the long lead II rhythm strip — a P wave does precede each QRS complex with a fixed (and normal) PR interval — so there is at least some conduction.

  • In general — the best lead for identifying atrial activity is lead II. Lead II provides the extra advantage of telling us if there is or is not sinus rhythm. The P wave should always be upright in lead II if there is a sinus rhythm. The only exceptions to this general rule — is if there is dextrocardia or lead reversal.
  • That said — there are times when atrial activity is seen better in other leads. In my experience — the 2nd-best lead for viewing atrial activity is lead V1. This is followed by leads III, aVR, aVF — and then taking a quick look at the remaining 7 leads.

  • What did YOU see in lead V1?

Additional Atrial Activity:

Although it would be easy to overlook additional atrial activity if one only looked at the long lead II rhythm strip — Lead V1 clearly tells us that there are 2 equally-spaced P waves for each QRS complex (RED arrows in Figure-2).

  • The fact that these P waves in lead V1 are equally spaced (RED arrows) — tells us that the underlying sinus rhythm continues throughout the tracing. There is 2:1 AV block (ie, 2 P waves for each QRS) — which defines the rhythm as some form of 2nd-Degree AV Block.
  • Since the ventricular rate is 54/minute — the atrial rate is twice this, or 108/minute.
  • The reason the 2nd P wave may not have initially be seen in the long lead II rhythm strip — is that it was hidden within the preceding T wave (WHITE arrows in the long lead II).
  • Although the 2nd P wave within each R-R interval is easiest to recognize in lead V1 — other leads also suggest this (ie, RED & WHITE arrows in lead V5).

  • PEARL #1: Use of calipers makes it easy to confirm regularity of the underlying atrial rhythm. Thus rules out entities such as atrial bigeminy (in which every-other-P-wave is a PAC). That said — it is common to see slight variation in the P-P interval in patients with 2nd- or 3rd-degree AV block. This is called a ventriculophasic” sinus arrhythmia. Most of the time this entity can be recognized by the fact that the P-P interval that “sandwiches” a QRS complex tends to be slightly shorter than the P-P interval that does not contain a QRS complex within it (thought to be due to slightly improved circulation from the cardiac output generated by the QRS within the 2 P waves that initiates mechanical contraction).

Figure-2: I've added RED and WHITE arrows to indicate the location of regular atrial activity (See text).

What About Your Interpretation of the 12-Lead ECG?

Now that we have defined the rhythm in Figure-2 as sinus with 2nd-Degree AV Block and 2:1 AV Conduction — there remains the question of how to interpret the rest of the 12-lead ECG.

  • As stated — the QRS complex is wide (probably ~0.12 second in Figure-2). QRS morphology is consistent with complete RBBB (ie, RBBB “Equivalent” Pattern in the form of a QR in lead I — and wide terminal S waves in both leads I and V6).
  • There is also LAHB, based on the predominantly negative QRS complexes in each of the inferior leads. Therefore, there is bifascicular block ( = RBBB/LAHB).
  • There is also evidence of prior infarctions. The lack of an initial r wave in lead III (ie, Qr pattern) — is not the result of simple LAHB, and indicates prior inferior infarction at some point in time.

  • PEARL #2: It is often difficult to distinguish between LAHB with or without prior inferior infarction. This is because the initial depolarization vector with each of these entities is “opposing” — such that the initial r wave with LAHB may prevent inscription of the Q wave of inferior infarction — and — the Q wave of inferior infarction may prevent inscription of the initial positive deflection (r wave) with the hemiblock. That said, in today’s case — the CLUES that tell us that both LAHB and prior inferior infarction have occurred at some point in time are: i) The wide initial Q wave in lead III (which should not be there with simple LAHB); ii) Fragmentation of the QRS in both leads II and aVF (ie, the extra “notching” on the upslope of the S wave) — and the r’ that we see in lead III (ie, normally with simple LAHB, there is an rS pattern in all 3 inferior leads — and not a Qr as we see here).

  • PEARL #3: There has also been anteroseptal infarction at some point in time — as seen by the large Q waves in numerous chest leads. With simple RBBB — there should be a triphasic (rsR’ or rSR’) complex in lead V1. The deep, wide Q wave we see here in lead V1 tells us that there has definitely been previous anteroseptal infarction.
  • Large Q waves, as well as additional fragmentation (notching) is also seen in leads V2, V3 and V4. In addition to extensive prior anteroseptal infarction — this patient clearly has significant coronary disease (ie, fragmentation in this clinical setting suggests extensive “scar”, from infarction and/or cardiomyopathy).
  • As to assessment of ST-T wave abnormalitiesnothing looks to be acute! Instead, there is nonspecific ST-T wave flattening — with slight-but-real ST elevation in leads V2, V3, V4. 

  • PEARL #4: Note that the ST segment in lead V1 is isoelectric. Normally with simple RBBB — the ST-T wave should be “oppositely-directed” to the last QRS deflection in the 3 KEY leads (ie, Since the last deflection in lead V1 is a positive R wave — there should normally be some ST-T wave depression in lead V1 when there is simple RBBB without any complicating factors). The fact that the ST-T wave in lead V1 is isoelectric instead of being at least slightly depressed is not "normal" with RBBB.

BOTTOM LINE: In addition to 2nd-Degree AV Block with 2:1 AV conduction — there has been inferior and anteroseptal infarction at some point in time. Although there is some ST elevation in leads V2,V3,V4 (and some inappropriate ST segment flattening in lead V1) — this is minimal. Other leads show nonspecific ST-T wave flattening and shallow T inversion in V5,V6 — so none of this looks acute. Instead — the slight ST elevation may reflect a left ventricular aneursym


The CASE Continues:

ECG #2 was obtained 15 minutes after ECG #1 (See Figure-3).


  • What has happened in the 15 minutes since ECG #1?

  • Has the “degree” of AV block improved?
  •     HINT: WHY did I calculate the atrial rate in each tracing?

Figure-3: ECG #2 was obtained 15 minutes after ECG #1. What has happened during these 15 minutes?


There is no longer 2:1 AV conduction in ECG #2. Instead — there is sinus rhythm with 1:1 AV conduction (RED arrows) — and a PVC ( = beat #6).

  • I suspect that an on-time sinus P wave is hidden within the ST-T wave of beat #6 in ECG #2.
  • There has been essentially no change in QRS morphology or in ST-T wave appearance between the 2 tracings.
  • The atrial rate has slowed slightly in ECG #2 (ie, from 108/minute — to 95/minute).

PEARL #5: Often ignored is the potential effect that the atrial rate may have on AV conduction. In today’s case — it is likely that the “degree” of AV block was not “worse” in ECG #1. Instead — it may simply be that the diseased AV node (in this older patient who obviously has severe underlying heart disease) may be able to conduct 1:1 at a sinus rate of 95/minute — but when the atrial rate speeds up a little (ie, to 108/minute) — it is only able to conduct 1 out of every 2 sinus impulses to the ventricles.

  • Given the history of syncope in this older patient — and the presence of bifascicular block (RBBB/LAHB) with prior infarctions — and periods of 2:1 AV Block — a permanent pacemaker may be needed. 
  • Ongoing ECG monitoring may facilitate documenting the need for a pacemaker. 
  • Echocardiography and cardiac catheterization may be indicated looking for LV aneurysm — determining LV function — and to clarify the anatomy in the event that there may be “fixable” coronary disease that might improve the patient’s conduction system disease.

Final PEARL: We can not distinguish with certainty between the Mobitz I and Mobitz II types of 2nd-Degree AV Block when there is 2:1 AV conduction. This is because we never see 2 consecutively conducted beats in a row — which means that we never get to see whether the PR interval would increase prior to dropping a beat IF given a chance to do so (as would be typical for the Mobitz I form of 2nd-degree AV block).
  • Mobitz I is far more common than Mobitz II. That said — when the QRS complex is wide — the PR interval of conducted beats is normal — and the patient clearly has significant underlying structural heart disease (as is seen in today's case) — then the chance that the conduction defect is Mobitz II increases. That said, regardless of whether the block is Mobitz I or Mobitz II — permanent pacing may still be needed in this patient for all of the reasons mentioned earlier.


Acknowledgment: My appreciation to 유영준 (from Seoul, Korea) for making me aware of this case and allowing me to use this tracing.


Relevant ECG Blog Posts to Today's Post:
  • ECG Blog #204 — Reviews the ECG diagnosis of BBB (reviewed in the Video Pearl).
  • ECG Blog #203 — Reviews a user-friendly approach to the Hemiblocks and to Bifascicular Block.

  • ECG Blog #236 — Reviews the 3 types of 2nd-Degree AV Block.

  • ECG Blog #271 — Reviews the concept of diffuse subendocardial ischemia.
  • ECG Blog #162 — Reviews a case of LBBB with acute STEMI.
  • ECG Blog #221 — How to diagnose acute MI when there is RBBB (reviewed in the Audio Pearl).
  • ECG Blog #298 — Reviews a case of RBBB/LAHB + Post. MI.