Tuesday, May 31, 2022

ECG Blog #309 — Syncope and Wellens?


The ECG in Figure-1 was obtained from a middle-aged man — who presented to the ED (Emergency Department) with syncope. No other clinical information available.

  • How would YOU interpret this ECG?
  • In view of this history — what are your diagnostic considerations?


Figure-1: ECG obtained from a middle-aged man with syncope.



MY Thoughts on the ECG in Figure-1:
The rhythm is sinus at ~65/minute. 

  • Regarding Intervals: The PR interval is normal. The QRS complex is not wide. However,  the QTc appears to be at least slightly prolonged (taking into account the relatively slow rate — and some uncertainty where to define the end point of the T wave given its biphasic appearance with terminal positivity in a number of leads).
  • Axis: Normal (about +40 degrees).
  • Chamber Enlargement: Obvious LVH (Left Ventricular Hypertrophy) — but no sign of other chamber enlargement. 


NOTE: The increase in R wave amplitude in some of the leads in Figure-1 is about as marked as you will ever encounter (ie, R wave amplitude attains ~50 mm in leads V4, V5). For clarity — I’ve used different colors to shade in QRS complexes in those leads in which voltage overlap is greatest (Figure-2).

  • Sugggestion: The amount of voltage overlap seen in Figure-1 complicates interpretation because of how difficult this makes it to determine where one QRS complex ends — and the next begins. Immediately repeating the ECG at HALF-standardization resolves the issue.


Regarding Q-R-S-T Wave Changes:

  • Q Waves: A small and narrow q wave is seen in lead III.
  • R Wave Progression: The R wave becomes predominant already in lead V2 (YELLOW outline of the QRS in this lead) — thus transition occurs early (ie, between leads V1-to-V2).

  • ST-T Waves Changes: There is diffuse and exceedingly deep, symmetric T wave inversion. ST segments in most leads are coved in shape — with several millimeters of J-point ST depression in those leads with very tall R waves. Isolated leads show modest ST elevation (ie, leads III, aVR, V1, V2) — but the predominant finding is clearly the ST coving with J-point depression and the very deep, symmetric T wave inversion.


PEARL #1: In a similar way that modified-Smith-Sgarbossa criteria incorporate the concept of “proportionality” into decisions about whether with LBBB, the amount of J-point elevation or depression is excessive (ECG Blog #282)this same concept is applied to Figure-2. That is, when assessing the size of the giant inverted T wave in lead V4 (that attains 20 mm in depth!) — We need to consider this in the context of the huge R wave in this same lead V4 that exceeds 50 mm in amplitude!

Figure-2: I've colored in selected QRS complexes in those leads in which voltage overlap is greatest (See text).


Putting It All Together:
The patient in today’s case is a middle-aged man who presented with syncope. No other information available. The principal findings in his initial tracing include sinus rhythm — marked LVH — diffuse ST segment coving with J-point depression and diffuse, symmetric T wave invertion, including a number of exceedingly deep T waves measuring 15-20 mm in depth. Even considering the marked increased in QRS amplitude — these are Giant" T-waves.

  • I’ve previously reviewed a number of cases in which there are Giant T Waves (See ECG Blog #276Blog #277and Blog #59). For clarity — I’ve reproduced in Figure-3 a summary defining “Giant” T waves, and listing the common causes that should be considered whenever you encounter this finding.


Giant T-Wave Syndrome
The designation of "Giant" T waves is reserved for a limited number of clinical entities that are likely to produce truly deep (>5-10 mm amplitude) T wave inversion.
  • The definition of "Giant" T waves is easily satisfied for the tracing in Figure-2 by the 15-20 mm depth of multiple T waves. 
  • Truly "giant" T waves are not overly common. The advantage of identifying this entity — is that doing should immediately suggest the diagnostic considerations listed in Figure-3.

  • While impossible to determine which of the entities listed in Figure-3 is (are) most likely in today's case — the relatively modest amount of QTc prolongation would seem to make a severe CNS disorder and Takotsubo Cardiomyopathy less likely. Ischemia is clearly a possibility given symmetric T wave inversion with J-point ST depression — but no mention of chest pain in the history makes this less likely.

  • My Suspicion: The overwhelming finding on today's tracing is the huge R wave amplitude in multiple leads. This strongly suggests that some form of hypertrophic cardiomyopathy is contributing (of which Apical Cardiomyopathy is the most common hypertrophic cardiomyopathy associated with Giant T waves).

Figure-3: Summary of the ECG criteria for "Giant" T Waves — with a list of the most common diagnostic entities to consider (See text).



QUESTION:
For clarity — I've reproduced the initial ECG in today's case in Figure-4.
  • Doesn't the steep descent of the T wave in lead V2 look like the picture of Wellens' Syndrome?

Figure-4: I've reproduced Figure-1, which shows the initial tracing in today's case. Doesn't steep descent of the T wave in lead V2 resemble the ECG picture of Wellens' Syndrome?


ANSWER:
It is tempting in Figure-4 — to interpret the slightly elevated ST segment with steep descent of the T wave in lead V2 as suggestive of Wellens' Syndrome. That said — Wellens’ Syndrome is unlikely to be present in today's case
  • While acute coronary disease is a definite possibility when there are Giant T waves (ie, acute ischemia is included among the entities listed in Figure-3) — it is well to remember that there are other causes of the ST-T wave picture seen in lead V2 of Figure-4. These include (among others) — LVH, cardiomyopathy, coronary reperfusion. 

  • In Figure-4 — I suspect the reason for the slight ST elevation, followed by steep descent of the T wave in lead V2 — is simply a reflection of the overall increased QRS and ST-T wave amplitude that we see, with lead V2 representing a “transition lead” placed between the ST elevation with upright T wave that we see in lead V1and — the J-point ST depression with very deep negative T wave that we see in lead V3.

  • PEARL #2: Remember the following KEY points about the ECG diagnosis of Wellens' Syndromei) A history of recent chest pain that has now resolved is an essential part of the diagnosis; ii) R wave amplitude in the anterior leads is markedly increased (ie, the R wave in lead V2 is ~15 mm). Most cases of Wellens' Syndrome are associated with reduced anterior R wave amplitude, often with delayed (not early) transition in the chest leads; iii) T wave inversion is not nearly so widespread in Wellens' Syndrome, as it is here; and, iv) There is marked LVH! The diagnosis of Wellens' Syndrome is far less reliable when there is LVH with LV "strain".

  • NOTE: For more on what Wellens' Syndrome is and is notSee ECG Blog #254



CASE Follow-Up:
The patient in today's case was found to have AHC (Apical Hypertrophic Cardiomyopathy — also known as Yamaguchi Cardiomyopathy). No other explanation for his syncope was detected. He was discharged from the hospital on ß-blocker therapy.
  • AHC is an uncommon variant of HCM (Hypertrophic CardioMyopathy). It was first described in Asian patients — and is still more prevalent in this population.
  • While AHC is most often a hereditary condition — not all patients have a positive family history.
  • The clinical course of AHC is highly variable. Patients may be asymptomatic (with AHC discovered incidentally when an ECG showing similar findings as in today's case is done for some other reason). Alternatively — patients may present with palpitations, dyspnea, cardiac-sounding chest pain — or — with otherwise unexplained syncope.
  • Although many patients with AHC do well — there is potential for adverse cardiac outcome (including cardiac arrest from malignant arrhythmias). As a result — Risk Stratification of patients detected with AHC is recommended to determine potential need for an ICD (Implantable Cardioverter Defibrillator).

  • For Review of AHC — See Kasirye et al (Clin Med & Research 10: 26-31, 2012) — and — Yusuf et al (World J Cardiology 3: 256-259, 2011).


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Acknowledgment: My appreciation to Mubarak Al-Hatemi (from Qatar) for the case and this tracing.
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Related ECG Blog Posts to Today’s Case: 

  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
  •  
  • ECG Blog #245 — Reviews the ECG diagnosis on LVH (with a 9-minute Audio Pearl in this post on this topic).
  •  
  • ECG Blog #254 — Reviews what Wellens' Syndrome is — and what it is not (with a 7:40 minute Audio Pearl in this post on this topic).
  •  
  • ECG Blog #46 — Reviews ECG findings with Takotsubo Cardiomyopathy.
  •  
  • ECG Blog #276 — Works through the differential diagnosis of Giant T Waves.
  • The June 22, 2020 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) reviews the case of Giant T-Waves with prolonged QTc that is shown in the TOP panel of Figure-5 above.





Friday, May 27, 2022

ECG Blog #308: Funny P Waves & Acute Inf. STEMI


The ECG in Figure-1 was obtained from a 70-year old man with longstanding hypertension. The patient was in for his yearly check-up. He denied symptoms.

  • A preliminary diagnosis of an acute inferior STEMI was made on seeing the ECG in Figure-1. Do you agree?


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


MY Thoughts on the ECG in Figure-1:
Beginning with Rate & Rhythm — the long lead II rhythm strip shows the rhythm to be regular at ~80-85/minute. The QRS complex is narrow. A P wave is seen before each QRS complex  — but this P wave is negative in lead II. Therefore the rhythm is not sinus. Instead — this is either a low atrial rhythmor — an accelerated junctional rhythm.
  • NOTE: Despite short duration of the PR interval — this does not distinguish been a low atrial vs junctional rhythm because it is speed of conduction (rather than distance from the SA node) that determines PR interval duration.


Continuing with Interpretation of ECG #1:

  • Intervals: The QRS and QTc intervals are normal.
  • Chamber Enlargement: None.
  • Q-R-S-T Changes: There is an isolated but large Q wave in lead III. R wave progression is normal — with transition (where the R wave becomes taller than the S wave is deep) occurring normally between leads V3-to-V4. The principal finding of concern is what appears to be ST elevation in each of the inferior leads — with what appears to be reciprocal ST depression in lead aVL. The rest of the ECG is unremarkable.



QUESTION:

  • Is the ST elevation in Figure-1 a "real" finding?





ANSWER: The Emery Phenomenon

The appearance of ST elevation in the inferior leads of Figure-1 reflects the Emery Phenomenon — in which the oppositely-directed atrial repolarization wave (ie, the T of the P wave) produces a "pseudo"-ST elevation effect because of the relatively large size of the negative inferior lead P waves, with short PR interval.
  • Most of the time — the Tp (also known as the "Ta" or atrial T wave) is hidden within the QRS complex. But on those uncommon occasions when a large negative P wave with short PR interval is seen in the inferior leads — the resultant oppositely-directed Tp may simulate acute inferior infarction (See My Comment in the June 3, 2020 post in Dr. Steve Smith's ECG Blog for discussion of the Emery Phenomenon in the context of a case that went to cath because of this "pseudo"-ST elevation).


To illustrate this phenomenon — I’ve adapted Figure-2, which I’ve taken from a 2015 post on the ECG Rhythms website.
  • As suggested in Figure-2 — the atrial repolarization wave (ie, the T of the P wave) is always present — but with sinus rhythm, the timing of the Tp will largely coincide with the timing of the QRS complex, and therefore not be noticed on the ECG (dotted RED half circle, seen to the left in Figure-2).
  • As shown in Figure-2 — the Tp will be oppositely directed to the P wave. Therefore, with normal sinus rhythm (in which by definition, the P wave will be upright in lead II) — the TP will be negative.
  • IF the P wave in lead II is negative (as may occur with either a low atrial or junctional rhythm) — then the Tp will be upright (dotted RED half circle, seen to the right in Figure-1). If the Tp wave is large in size and upright — it may distort the end of the QRS complex, and produce the false impression of ST elevation.

Figure-2: Illustration of the Emery Phenomenon. (I have adapted this Figure from the 2015 post by Dr. Bojana Uzelac on Armel Carmona’s ECG Rhythms website).


KEY Points:
  • The size of the Tp wave will be proportional to the size of its P wave. A small P wave will produce a correspondingly small Tp wave. A large P wave will produce a much bigger Tp wave.
  • Actually, the effect of the oppositely-directed atrial repolarization wave ( = the Tpalso known as the "Ta" or atrial T wave) will be even larger than shown above in Figure-2 — because normal duration of the Ta wave is significantly longer (up to 2-3 times longer) than normal P wave duration (Francis). This may account for an exaggerated effect on the ST segment when the P wave is large.
  • That said — I preserved the same relative proportions in Figure-2 as were seen in the original version of this Figure taken from the ECG Rhythms website. Note that the PR interval for the negative P wave in Figure-2 is almost as long as the PR interval for normal sinus rhythm. But IF the PR interval for the negative P wave in lead II is much shorter (as occurs in today’s case) — then the upright Tp wave that will be seen with a low atrial rhythm will be further displaced to the right, which will produce a much greater degree of pseudo-ST-elevation!



The CASE Continues:

10 minutes later in today's case — a repeat ECG was done (Figure-3).

  • What has happened in Figure-3?


Figure-3: Comparison between the initial ECG — and the repeat ECG done 10 minutes later.


ANSWER:
The repeat ECG (bottom tracing in Figure-3) — shows return of normal sinus rhythm with an upright P wave in lead II, and an overall slower heart rate than was seen in ECG #1.
  • Following this return of the normal upright sinus P wave in lead II (as well as in the other inferior leads) — there is no longer any ST elevation in the inferior leads of ECG #2. In addition — the small amount of J-point ST depression that had been seen in lead aVL of ECG #1 is no longer present.

  • Since ECG #2 was obtained just 10 minutes after ECG #1, without any change in the patient's clinical condition — this resolution of inferior lead ST elevation (and of the J-point ST depression in lead aVL) — confirms that the ST elevation that had been seen in ECG #1 was not real. Instead — it was simply an effect of the Emery Phenomenon, brought about as a result of the large-amplitude negative inferior lead P waves with short PR interval that were seen in ECG #1.

KEY Point:
  • Although there is no longer any ST elevation in ECG #2 — the T waves in the inferior leads still look "hypervoluminous" (ie, each of the inferior lead T waves either equal or exceed amplitude of the R wave in the same lead — and each of these T waves have a broader-than-expected base).
  • In addition — despite a QRS complex in lead aVL that is not predominantly negative — the T wave in this lead is still inverted.

  • PEARL: The importance of the History can not be overstated. IF I was shown ECG #2 and told that the patient with this ECG was complaining of new-onset chest pain — I would interpret this tracing as showing hyperacute T waves in each of the inferior leads, with reciprocal change in lead aVL. My diagnosis would be acute RCA (Right Coronary Artery) occlusion until proven otherwise.

  • However, the 70-year old man in today's case was completely asymptomatic — with the reason for getting an ECG being "routine", as part of this patient's regular check-up. In view of this information — it is highly likely that nothing acute is going on in ECG #2.
  • I suspect that review of this patient's medical record, looking for a previous ECG for comparison would quickly resolve all questions by showing a longstanding similar ST-T wave appearance.

Take-Home MESSAGE:
Be aware of the Emery Phenomenon! All providers whose work entails ECG interpretation will occasionally encounter patients with a low atrial or junctional rhythm (with large negative P waves and a short PR interval in the inferior leads) that produces inferior lead ST elevation (often with reciprocal change in lead aVL) that simply is not real.


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Acknowledgment: My appreciation to Kianseng Ng (from Kluang, Malaysia) for the case and this tracing.
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Additional Relevant Material to Today's Case:
  • See ECG Blog #185 — for review of the Systematic Ps, Qs, 3R Approach to rhythm interpretation.
  • See ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.

  • For more on distinction between Low Atrial vs Junctional Rhythm — Please see My Comment at the BOTTOM of the page in the January 28, 2019 post in Dr. Smith's ECG Blog.

  • See ECG Blog #290 — for another example of the Emery Phenomenon.
  • And for another case of the Emery Phenomenon — Please see My Comment at the BOTTOM of the page in the June 3, 2020 post in Dr. Smith's ECG Blog.





Monday, May 23, 2022

ECG Blog #307 — No Symptoms, But a Slow Rate


The ECG in Figure-1 — was obtained from a man in his 40s, who was referred to the ED (Emergency Department) for a "slow rhythm". The patient was asymptomatic at the time this ECG was recorded.
  • How would YOU interpret this rhythm?
  • What are your diagnostic considerations?

Figure-1: 12-lead ECG and long lead rhythm strip recorded on an asymptomatic man in his 40s.


My Thoughts on Figure-1:
Intuitively applying the Ps, Qs, 3R Approach for assessment of the rhythm in Figure-1 (See ECG Blog #185)my initial impression of this tracing (that I made within the first ~15 seconds of seeing this ECG) — was the following:
  • There is a slow, supraventricular (narrow QRS) rhythm .
  • This rhythm is irregular.
  • There is some variation in QRS morphology (seen best in the long lead V1 rhythm strip). 
  • P waves are present — and at least some of these P waves are not conducting.
  • In a quick overall glance at this 12-lead tracing — there do not appear to be acute ST-T wave changes (at least nothing that might require prompt cath or thrombolytic treatment).

  • NOTE: The clinical goal of this quick initial look at today's tracing is meant to see IF there are any priorities that need to be immediately addressed. That said — since this patient was asymptomatic (therefore hemodynamically stable) — it is likely that he has been in this rhythm for at least some period of time — and by definition, this provides us with a moment for more careful analysis.

PEARL #1: In applying the Ps, Qs, 3R Approach — I have found the simple act of identifying all P waves to be invaluable for guiding me toward the right diagnosis.
  • Using calipers greatly facilitates identifying all of the P waves (including those partially or totally hidden within the QRS or ST-T wave of certain beats).
  • The P waves are small everywhere in Figure-1. That said — they are BEST seen in the long lead II rhythm strip. Setting calipers at the P-P interval between any 2 P waves that are clearly seen in the long lead II rhythm strip — readily allows you to "walk out" this interval throughout the rhythm strip (RED arrows in Figure-2).

PEARL #2: It is common to see slight irregularity in the P-P interval in association with slow sinus rhythms (regardless of whether or not some degree of AV block is present). Awareness of this sinus arrhythmia facilitates finding sinus P waves that may be partially hidden (ie, such as the earlier-than-expected P wave seen immediately after the QRS complex of beat #6 in Figure-2).


CHALLENGE: Look at the RED arrows in Figure-2 that highlight all sinus P waves in this rhythm strip:
  • Are any of these P waves conducted to the ventricles? IF so — Which P waves in Figure-2 appear to be conducted?
  • Are there any P waves that you know are not being conducted?

Figure-2: I've added RED arrows to highlight sinus P waves.


ANSWER: 
For clarity in Figure-3 — I've modified the colors of the arrows in the long lead rhythm strip (from Figure-2) — to highlight P waves that most probably are not conducting.
  • The 3 P waves highlighted by the YELLOW arrows in Figure-3 are definitely not conducting. The first 2 of these arrows (ie, the YELLOW arrows in front of beats #1 and #4) — highlight P waves with a PR interval that is too short to conduct.
  • The 3rd YELLOW arrow in Figure-3 highlights a P wave that occurs immediately after beat #6. We know that this P wave is also not conducting — because it clearly falls within the absolute refractory period.

  • Of the remaining 6 P waves — the 2 P waves highlighted by the PINK arrows (that occur nearly midway between beats #3-4 and between #5-6)are highly unlikely to be conducted, because this would require an exceedingly long PR interval.

  • RED arrows highlight the remaining 4 P waves. Each of these remaining 4 P waves could be conducting.

PEARL #3: Perhaps the BEST clue that a P wave is being conducted to the ventricles — is when the same PR interval is seen before several beats.
  • In Figure-3the PR interval preceding beats #2, 5 and 7 is identical. Therefore — each of the P waves in front of these beats is being conducted to the ventricles. I measure this PR interval as slightly more than 1 large box in duration (ie, ~0.22 second) — so, consistent with 1st-degree AV block.

  • QUESTION: Isn't the PR interval preceding beat #3 slightly longer than the PR interval before beat #2?

Figure-3: I've labeled the P waves in today's rhythm with 2 additional colors.


Putting It All Together:
We have essentially "solved" the arrhythmia in Figure-3:
  • The underlying rhythm is sinus bradycardia and arrhythmia (with an overall ventricular rate ~50/minute). The PR interval of sinus-conducted beats is prolonged to 0.22 second — so there is 1st-degree AV block.

  • Some form of 2nd-degree AV block is present — because the on-time P waves highlighted by PINK arrows in Figure-3 fail to conduct despite having more than adequate opportunity to do so.
  • The type of 2nd-degree AV block is Mobitz I (AV Wenckebach) — because in the one group of beats in which there are 2 consecutive P waves that do conduct, the PR interval progressively increases until a beat is dropped (ie, the PR interval before beat #3 is longer than the PR interval before beat #2 — and then the next on-time P wave highlighted by the PINK arrow after beat #3 is not conducted).
  • Other features consistent with the Mobitz I form of 2nd-degree AV block in Figure-3 include: i) Statistics = The clinical reality that over 90-95% of all 2nd-degree AV blocks are of the Mobitz I type; ii) The QRS complex is narrow (whereas it is usually wide with Mobitz II); and, iii) Sinus-conducted beats manifest 1st-degree AV block (whereas it is more likely that the PR interval of conducted beats with Mobitz II will be normal).

  • Clinically The importance of distinguishing between the Mobitz I and Mobitz II forms of 2nd-degree AV block — is that patients with Mobitz II are much more likely to need a pacemaker (See LINKS and the ADDENDUM below for more on the ECG diagnosis and clinical implications of the AV blocks).

What Then are Beats #1, 4 and 6?
We have emphasized that the P waves highlighted by YELLOW arrows in front of beats #1 and #4 have a PR interval that is too short to conduct. No P wave immediately precedes beat #6. Therefore — none of these beats are sinus-conducted.
  • Since the QRS complex of beats #1, 4 and 6 is narrow — these beats are not ventricular in etiology.
  • By the process of elimination, since beats #1,4,6 are neither sinus-conducted nor ventricular in etiology — they must be "escape" beats arising either from the AV node or from the Bundle of His. Because the R-R interval preceding beats #4 and #6 is long (ie, ~10 large boxes in duration — corresponding to an escape rate of ~30/minute) — these beats probably originate from "lower down" in the conduction system (ie, from the Bundle of His).
  • In support of a His origin for these escape beats — is the decidedly different QRS morphology of beats #1, 4 and 6 in the long lead rhythm strips. While QRS morphology of junctional escape beats may differ slightly from QRS morphology of sinus-conducted beats — there usually is not as marked of a difference in morphology as we see in Figure-3.

PEARL #4: Although it is fairly easy to tell which P waves are (and are not) being conducted to the ventricles in Figure-3 — it is sometimes quite difficult to determine this. In such cases — recognizing slight variation in QRS morphology may provide an important clue that indicates which beats represent non-conducted "escape" beats — and, knowing this may greatly facilitate diagnosis of the rhythm etiology (See ECG Blog #63 for an example of this Pearl in action)


PEARL #5: It is important to realize that there is transient AV dissociation in Figure-3. That is — None of the P waves highlighted by the YELLOW arrows are related to neighboring QRS complexes (because none of these P waves are conducted to the ventricles).
  • This serves to illustrate that AV dissociation is not the same thing as complete AV block. The fact that no less than 4 of the P waves in Figure-3 are conducted to the ventricles rules out the possibility of complete AV block (in which none of the P waves would be conducted to the ventricles).

  • For more on distinction between AV dissociation vs complete AV block — See ECG Blog #191.


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The Laddergram:
For clarity — I've drawn a laddergram in Figure-4 of today's case, to illustrate the mechanism of this arrhythmia.

Figure-4: Laddergram of today's case. Mobitz I 2nd-degree AV block is diagnosed by progressive increase in the PR interval (from beat #2-to-beat #3) — until the P wave after beat #3 is blocked. Beats #1, 4 and 6 are "escape" beats. Although I drew these "escape" beats as originating from within the AV Nodal Tier — they may well originate from a lower level in the conduction system (ie, from the Bundle of His).


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CASE Conclusion:
Surprisingly, the 40-ish year old man in today's case was not symptomatic at the time he presented with his initial ECG (which I've reproduced in Figure-5).
  • Presumably — the reason he came to the ED, was that someone noted a slow and irregular pulse.
Figure-5: The initial ECG in today's case. P waves are labeled with RED arrows.


WHY Did this Patient Present with Asymptomatic Mobitz I?
It is not common for patients to present with significant bradycardia and 2nd-degree AV block without any symptoms — especially in the younger adult age group of today's patient. As a result — this case presentation should raise a number of questions:
  • Was the patient truly asymptomatic? Many patients deny or ignore symptoms — so a careful history in hope of discovering clues to the rhythm etiology is essential.
  • The most likely etiology for a bradycardia with Mobitz I, 2nd-degree AV block — would seem to be a myocardial infarction that the patient was somehow unaware of. While the ECG in Figure-5 does not show obvious signs of recent or acute infarction — there are some subtle ECG findings. These include: i) A hint of ST segment coving and elevation in the 1 QRST complex that we see in lead aVL (corresponding to beat #3); and, ii) A taller-than-expected R wave appears in lead V3. These 2 findings could be consistent with recent postero-lateral infarction — though they are in no way definitive. Other leads show no more than nonspecific ST-T wave flattening.

  • Additional considerations for entities that might result in Mobitz I, 2nd-degree AV block are shown in Figure-6. If nothing in a careful history and thorough evaluation of this patient suggests any of these entities — cardiac cath should be considered, looking for underlying "silent" coronary disease that might be amenable to reperfusion.
  • If nothing "fixable" is found — a pacemaker may ultimately be needed if there is further slowing of the overall ventricular rate and/or if symptoms develop.

Figure-6: Diagnostic considerations for a patient who presents in AV block (adapted from Mangi et al — StatPearls, 2021).




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Acknowledgment: My appreciation to Mubarak Al-Hatemi (from Qatar) for the case and this tracing.
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For MORE on Diagnosis of ABlocks/AV Dissociation:
  • ECG Blog #185 — Reviews the Ps, Qs, 3R Approach to Rhythm Interpretation.

  • ECG Blog #188 — for Review on How to Read (and Draw) Laddergrams.

  • ECG Blog #63 — Reviews a case of Mobitz I with Junctional Escape.

  • ECG Media Pearl #4 (4:30 minutes Audio— The AV Blocks & WHEN to Suspect Mobitz I — See ECG Blog #186 —
  • ECG Media Pearl #(12:00 minutes Video ECG Blog #189 — What type of AV Block? Detailed analysis of this challenging arrhythmia (including ECG Video with step-by-step analysis of this complex laddergram).

  • ECG Media Pearl #8 (8:20 minutes Video) — ECG Blog #191 — Distinguishing between AV Dissociation vs Complete AV Block.
  • ECG Media Pearl #9 (5:40 minutes Video) — ECG Blog #192 — Reviews the 3 Causes of AV Dissociation.

  • ECG Media Pearl #19 (5:00 minutes Audio) — ECG Blog #202 — How to quickly rule out complete AV Block within seconds!
  • ECG Media Pearl #41 (4:00 minutes Audio) — ECG Blog #224 — Reviews HOW to recognize Mobitz I within seconds when there is ongoing Inferior STEMI.



ADDENDUM (5/23/2022):
This 15-minute ECG Video — Reviews the 3 Types of 2nd-Degree AV Block — plus — the hard-to-define term of "high-grade" AV block. I supplement this material with the following 2 PDF handouts.
  • Section 2F (6 pages = the "short" Answer) from my ECG-2014 Pocket Brain book provides quick written review of the AV Blocks (This is a free download).
  • Section 20 (54 pages = the "long" Answer) from my ACLS-2013-Arrhythmias Expanded Version provides detailed discussion of WHAT the AV Blocks are — and what they are not(This is a free download).
  • Mobitz I ( = AV Wenckebach).
  • Mobitz II.
  • 2nd-Degree AV Block with 2:1 AV conduction.







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).

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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.

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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.

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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!
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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. 


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