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).
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• 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).
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• 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. 
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• 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.

CONFESSION:

While labeling today's ECG for Figure-2 — I 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?
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• 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.
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• 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).
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• 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.
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• 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).

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

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Relevant ECG Blog Posts to Today's Post:

• ECG Blog #185 — Reviews the Ps, Qs, 3R Approach to Rhythm Interpretation.
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• 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).
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• 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.

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.

QUESTIONS:

• 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).
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• 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).
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• 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.
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• 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.
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• 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!
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• 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.

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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.
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• 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.
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• 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).
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• 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 (Remember — it 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".

My Clinical IMPRESSION:

• 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.
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• 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.
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• 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!

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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?
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• 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!

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

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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.
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• ECG Blog #236 — Reviews the 3 types of 2nd-Degree AV Block.
• ECG Blog #192 — Reviews the 3 causes of AV Dissociation.
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• 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.
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• ECG Blog #188 — Reviews all about Laddergrams!
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• ECG Blog #185 — Use of a Systematic Approach to Rhythm Interpretation. 
• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
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• 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.
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• ECG Blog #262 — Acute 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.
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• ECG Blog #188 — How to Read (and Draw) Laddergrams. 

ECG Blog #303 (EQC) — The Patient Fainted

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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.

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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.

QUESTIONS:

• 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).
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• 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.
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• 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).
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• 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 abnormalities — nothing 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. 

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The CASE Continues:

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

QUESTIONS:

• 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?

ANSWERS:

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.

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

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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.

ECG Blog #302 (QC) — An ECG Quick Case ...

NOTE (5/2/2021): 

I'm adding a feature to my ECG Blog — namely, some ECG "Quick Cases" ( = EQCs) — in which I'll provide "quick answers" to short ECG cases, with my impression of the "essentials" that come to me within the first few seconds that I see the tracing.

• While I always encourage a systematic approach to ECG assessment — my goal is to help expedite clinical decision-making.
• I'll add LINKS at the bottom of each case where more detailed discussion can be found on related cases.

— I WELCOME your feedback on this new feature! —

— Ken Grauer, MD (ekgpress@mac.com) —

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The ECG in Figure-1 was obtained from a patient with chest pain.

• How would YOU interpret this tracing?

Figure-1: ECG obtained from a patient with chest pain.

MY Thoughts on the ECG in Figure-1:

The rhythm is sinus at ~80/minute. The PR interval is normal. The QRS is wide (I measure the QRS to be at least 0.14 second in duration).

• The most time-efficient way to interpret a sinus rhythm with a wide QRS — is to figure out WHY the QRS is wide before proceeding further. There are 3 Possibilities (ECG Blog #204). These are: i) RBBB; ii) LBBB; or, iii) Neither RBBB nor LBBB — which defines the reason for QRS widening as IVCD (IntraVentricular Conduction Defect).
• The 3 KEY leads to determine the type of conduction defect are left-sided leads I and V6 — and right-sided lead V1. The ECG in Figure-1 is consistent with complete RBBB because: i) There is an rSR' in lead V1; and, ii) There are upright R waves with a wide terminal S wave in lateral leads I and V6.

Resuming my systematic approach:

• Finishing "Intervals" — the QTc does not appear excessively prolonged given the presence of RBBB.
• There is no chamber enlargement.
• Q Waves: There is no more than a tiny q wave in lead V6.
• R Wave Progression: Not relevant given the RBBB.

ST-T Wave Changes:

Normally with RBBB — the ST segment and T wave are oppositely directed to the last QRS deflection in the 3 KEY leads:

• Instead of the expected ST-T wave depression that should normally be seen in lead V1 with RBBB (ie, oppositely directly to the last QRS deflection, which is the positive R' complex) — there is ST elevation in lead V1 (above the dotted RED line in this lead — See Figure-2).
• Instead of a purely upright T wave that should normally be seen in left-sided leads I and V6 with RBBB (ie, oppositely directed to the last QRS deflection, which is the negative wide terminal S wave) — there is a down-up biphasic T wave (BLUE — then RED arrows in these leads).
• Biphasic T waves are seen in a number of other leads (including leads II, aVL; V2-thru-V5). This is not a normal finding — and suggests ischemia.
• Normally with RBBB — the ST-T wave depression that is expected in anterior leads — does not continue into the lateral chest leads. It certainly should not increase, as it does here in lateral leads V5 and V6. ST depression should also not be seen in the limb leads as is seen here.
• The other lead that manifests ST elevation is lead aVR — which shows slightly more ST elevation than is seen in lead V1.
• The final finding of note in Figure-1 — is excessive fragmentation, in the form of extra notching that is most marked in leads V2, V3.

Figure-2: I've labeled the ECG in Figure-1 (See text).

Clinical IMPRESSION:

The ECG in Figure-1 shows sinus rhythm with QRS widening due to complete RBBB. The QRS is very wide and fragmented. There are abnormal biphasic T waves — diffuse ST depression beyond that expected for RBBB — and ST elevation in leads aVR and V1.

• This patient almost certainly has significant underlying heart disease. 
• The finding of ST depression with biphasic T waves in multiple leads, with ST elevation in lead aVR > V1 — strongly suggests diffuse subendocardial ischemia. Given the history of chest pain — cardiac cath is indicated to define the anatomy.
• This ECG picture does not suggest acute coronary occusion. But severe (possibly multi-vessel) coronary disease should be suspected until proven otherwise.

P.S. — I was asked if this ECG indicates prior "septal" infarction? Close observation of lead V1 reveals there is a very small-but-present initial positive deflection (r wave) in this lead — so although highly likely that this patient has significant underlying heart disease — we cannot make the diagnosis of "prior septal infarction" from this ECG alone.

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Relevant ECG Blog Posts to Today's Post:

• ECG Blog #204 — Reviews the ECG diagnosis of BBB (reviewed in the Video Pearl).
• 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.