ECG Blog #414 — What Kind of AV Block?

 

I was sent the ECG in Figure-1 — without the benefit of any history.

QUESTION:

• What kind of AV block is present in Figure-1? 

Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Approach to Today’s Tracing:

As always — I favor beginning assessment with a quick look at the long lead rhythm strips at the bottom of the tracing. By the Ps, Qs, 3R Approach (which I review in ECG Blog #185):

• P waves are present — and best seen in lead V1.
• The QRS complex is narrow in all 12 leads.
• The rhythm is not Regular. The ventricular Rate varies.
• The 5th parameter of the Ps,Qs,3R Approach — is the 3rd R, which recalls “Related” — or determining if P waves are (or are not) related to neighboring QRS complexes. This last parameter is best assessed by labeling P waves in the long lead V1 rhythm strip (which I have done in Figure-2).

QUESTIONS:

Take a LOOK at Figure-2 — in which RED arrows highlight the P waves. 

• How would YOU describe the regularity (or lack thereof) of P waves in today's rhythm?
• Are all of the P waves originating from the SA node?
• Are all P waves conducted to the ventricles?

Figure-2: I have labeled P waves with RED arrows in today's rhythm.

WHY are P waves so Irregular in Figure-2?

Now that we have labeled all P waves in Figure-2 with RED arrows — Isn't it much easier to appreciate the irregular irregularity of the atrial rhythm?

• Most of the time — it is lead II that provides best visualization of sinus P waves. That said — this is not the case in today's rhythm, in that lead V1 provides more consistent visualization of atrial activity in Figure-2.

What We Know about the Rhythm ...

• At least some of the P waves in Figure-2 appear to be sinus P waves that are conducted to the ventricles — namely the P waves before beats #3,7,8 and 9. I say this because each of these beats is preceded by a similar-looking P wave with a constant and normal PR interval.
• Other P waves are clearly not conducted to the ventricles — because the PR interval in front of beats #1,2,5,6 and 11 appears to be too short to conduct. The fact that the R-R intervals that precede these beats are virtually the same (ie, ~5 large boxes in duration) — suggests that beats #1,2,5,6 and 11 are all junctional escape beats at an appropriate AV nodal escape rate of ~60/minute (ie, between the usual 40-60/minute range expected with junctional escape).

I am less certain about the origin of beats #4 and 10 — because these beats occur so much earlier-than-expected. 

• The timing of beats #4 and 10 suggests that these beats may be PACs (Premature Atrial Contractions). Alternatively — it could be that each of the RED arrow P waves in Figure-2 is a sinus P wave that occurs in association with a very marked sinus arrhythmia. 
• PACs typically manifest a different P wave morphology than sinus-conducted P waves, depending on how near or how far the site of the PAC is with respect to the SA node. For example, PACs arising from very close to the SA Node — may look very similar to sinus-conducted beats in most (if not in all) 12 leads.
• Balanced with the above considerations regarding potential variation in P wave morphology — is the clinical reality that a certain amount of inherent variation in P wave morphology is common in sinus rhythms (See Pearl #6 in ECG Blog #413).
• 
  
• BOTTOM Line: I do not believe it possible to determine what the etiology of beats #4 and 10 is with any certainty from Figure-2. We simply cannot tell from this single tracing if the slight variability in P wave morphology that we see in lead II (not so much in lead V1) is "real" vs the effect of some normal variation in P wave morphology expected with sinus rhythms. 

Putting It All Together — in a Laddergram:

A picture "is worth 1,000 words" — so it's easier to illustrate the above description by means of a laddergram.

• As I note above — it's not possible from this single tracing to determine with any certainty if beats #4 and 10 represent PACs — vs participants in a marked sinus arrhythmia. For the purpose of simplicity (ie, of not having to assume the additional element of there also being PACs in today's rhythm) — I assumed all RED arrow P waves were sinus impulses (ie, beats #3,7,8,9 — also being sinus-conducted beats).
• Beats #1,2,5,6 and 11 represent junctional escape beats at an appropriate escape rate of ~60/minute (the P waves occurring just before these beats manifesting a PR interval too short to conduct).
• 
  
• NOTE: There is transient AV dissociation in today's rhythm — in the form of sinus P waves not related to neighboring QRS complexes (ie, the P waves before beats #1,2,5,6,11 manifesting a PR interval too short to conduct). As discussed in detail in ECG Blog #192 — there are 3 Causes of AV Dissociation: i) By "default"; ii) By "usurpation"; and, iii) As a result of AV block. Regardless of whether there is marked sinus arrhythmia vs short pauses following PACs — the cause of the transient AV dissociation seen in today's rhythm is a form of "default" — because the reason junctional escape beats #2,5,6 and 11 occur is a result of the slightly longer R-R intervals that precede each of these beats.
• BUT — there is no evidence of any AV block in today's tracing — because we never see on-time sinus P waves that should conduct, yet fail to do so. 
• 
  
• P.S. (Beyond-the-Core): We were not provided with any history in today's case. Another possible explanation for today's rhythm might be a marked increase in vagal tone (as per the case presented in ECG Blog #61) — which could result in not only marked sinus arrhythmia — but also some variation in the PR interval of sinus-conducted beats (ie, It looks like the PR interval before conducted beats #4 and 10 may be slightly longer than the PR interval of other sinus-conducted beats).

Figure-3: Laddergram illustration for today's rhythm. The laddergram suggests there is marked sinus arrhythmia — that results in transient AV dissociation by "default" because junctional "escape" beats #1,2,5,6,11 occur before the delayed sinus impulses have an opportunity to conduct. The junctional escape rhythm is set at ~60/minute, such that these junctional escape beats are appropriate (and do not represent any form of AV block! ).

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Acknowledgment: My appreciation to Danilo Franco (from Italy) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #185 — Reviews my System for Rhythm Interpretation, using the Ps, Qs & 3R Approach.
• ECG Blog #188 — Reviews how to read and draw Laddergrams (with LINKS to more than 90 laddergram cases — many with step-by-step sequential illustration).
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• ECG Blog #192 — The 3 Causes of AV Dissociation.

• ECG Blog #191 — Reviews the difference between AV Dissociation vs Complete AV Block.
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• ECG Blog #389 — ECG Blog #373 — and ECG Blog #344 — for review of some cases that illustrate "AV block problem-solving".
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• ECG Blog #267 — Reviews with step-by-step laddergrams, the derivation of a case of Mobitz I with more than a single possible explanation.
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• ECG Blog #61 — Vagotonic block. 

ECG #413 — A Pre-Op ECG in an ASx Patient

I was sent the tracing shown in Figure-1 — told only that this was a preoperative ECG obtained from an asymptomatic older woman scheduled for non-cardiac surgery.

• How would YOU interpret this ECG?
• Would you approve her for surgery if the procedure was nonemergent?  

Figure-1: Preoperative ECG from an asymptomatic older woman scheduled for non-cardiac surgery. Would you approve her for a nonemergent surgical procedure? (To improve visualization — I've digitized the original ECG using PMcardio).

MY Initial Thoughts on Today’s CASE:

This patient should not be approved for non-emergent surgery.

• Looking first at the long-lead II rhythm strip — there is significant bradycardia, with a heart Rate just under 40/minute. The QRS complex is narrow in all 12 leads — so the rhythm is supraventricular. 
• The overall ventricular response looks Regular.
• P waves are present — but they seem to be unRelated to neighboring QRS complexes (ie, The PR interval varies — at the least, for some of the beats).
• 
  
• BOTTOM Line: Since many of the P waves in this long lead II rhythm strip occur at points within the R-R interval where they appear to have more than ample opportunity to conduct — yet still fail to do so — some form of 2nd-degree (if not, 3rd-degree) AV block is present, in association with marked bradycardia.

Comment:

• PEARL #1: I arrived at the above initial thoughts on today’s rhythm within seconds of seeing the long lead II rhythm strip. Stressing this aspect of how time-efficiency in rhythm diagnosis may facilitate rapid clinical decision-making — is one of my primary objectives in writing this ECG Blog (ie, the surgeon in today’s case may be waiting on your interpretation of this “routine” pre-op ECG before proceding). 
• PEARL #2: The KEY for optimal time-efficiency — is to use a systematic approach that addresses the 5 parameters, which are easily recalled by the phrase, “Watch your Ps, Qs and the 3Rs” (See ECG Blog #185 for review of this system). Applying the Ps,Qs,3Rs tells us within seconds that this 70-year old woman should not be approved for non-emergent surgery.

What About the 12-Lead ECG?

While our brief assessment of the rhythm in today's case is enough to merit canceling this patient's non-emergent surgery — there is more!

• The 12-lead ECG is very concerning. Although we only see 1 or 2 beats in each lead (because the heart rate is so slow) — there is ST segment straightening with slight depression, that appears to be maximal in lead V3 (especially noteworthy since normally there is slight ST elevation in this lead!). ST segment straightening is also seen in leads I,aVL; and in leads V4,V5,V6 (with a hint of ST depression in leads V5,V6). Finally — the T waves in leads V4,V5,V6 are "fatter"-at-their-peak than they should be (beyond what might be expected from superposition of P waves on these T waves). KEY Point: Although the above ST-T wave changes are admittedly subtle — the fact that they are undeniably present in so many leads (and most marked in lead V3) is real!
• 
  
• PEARL #3: 2nd- and 3rd-degree AV blocks are a common complication of inferior and/or posterior OMI. As a result — the finding of ST segment flattening in multiple leads, but being most marked in lead V3 — in a patient with bradycardia and some significant form of AV block — suggests a strong possibility of recent posterior OMI (See ECG Blog #351).
• 
  
• PEARL #4: The fact that today's elderly patient was asymptomatic does not rule out the possibility of having had an acute (or recent) MI. As discussed in ECG Blog #228 — the incidence of "Silent" MI may be as high as between 20-40% of all MIs, being especially common in older individuals.

MY Impression of Today's CASE: Despite no symptoms — I strongly suspect from the initial ECG, that this older woman had a recent LCx (Left Circumflex) occlusion with posterior MI — that resulted in bradycardia with 2nd- or 3rd-degree AV block. Given the lack of symptoms — this was a “silent" MI. The patient may need a pacemaker.

• CASE Follow-Up: Providers in today's case recognized the above abnormalities — and promptly referred the patient to a PCI center for cardiac catheterization and potential pacemaker insertion.

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Looking Closer at Today's Rhythm:

The rhythm in Figure-1 has a number of complexities. As a result — I needed additional time before deciding on the precise rhythm diagnosis. I walk through my thought process below. But the point to emphasize — is that it should only take seconds to recognize that there is bradycardia from significant AV block.

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My Approach to Rhythm Determination:

• PEARL #5: The simple step of labeling P waves is tremendously helpful in facilitating rhythm diagnosis. I have done this with RED arrows in Figure-2.
• Prior to labeling the P waves — Did YOU Notice how much variation there is in P wave morphology?
• 
  
• Is the atrial rhythm in Figure-2 regular? If not — How does this realization complicate today's rhythm diagnosis?

Figure-2: I've labeled P waves with RED arrows.

PEARL #6: In Figure-2 — Isn't there a lot of variation in P wave morphology? This raises the question as to whether each of the RED arrow P waves is a sinus P wave? — OR — Is the underlying rhythm sinus with atrial bigeminy (ie, every-other-P-wave being a PAC?).

• NOTE: A certain amount of variation in P wave morphology is common in sinus rhythms — be this from patient (or electrode lead) movement — from artifact — or — from more complex factors that may include variation in the exit site of atrial depolarization from the SA node — variation in the impulse path through the atria and/or in the degree of intra-atrial conduction block (Qin et al: Circulation 139:1225-1227, 2019 — Pezzuto et al: EP Europace 20, 2018 — Platonov: Ann Noninvasive Electrocardiol 17(3):161-169, 2012).
• While acknowledging that a certain amount of variation in P wave morphology is often seen with sinus rhythms — there usually is not as much variation as is seen in Figure-2 (ie, from the fairly tall and pointed P wave before beat #5 — compared to the tiny, flat P wave in front of beat #6).
• 
  
• BOTTOM Line: The above said — I strongly suspect that despite marked variability in P wave morphology in today's tarcing — that all of the RED arrow P waves in Figure-2 are sinus P waves! I say this because of the PR and R-R intervals that I will measure momentarily in Figure-3 (ie, The PR interval continually varies — whereas it should be constant if the rhythm was sinus with atrial bigeminy).

PEARL #7: As is evident for many of the examples of AV block that have appeared in this ECG Blog — it is common to see a "ventriculophasic" sinus arrhythmia in association with 2nd or 3rd degree AV block. Much of the time (as is the case in Figure-2) — the shorter P-P interval is the one that “sandwiches” a QRS complex (the theory being that perfusion improves following ventricular contraction — with resultant shortening by a slight amount of the P-P interval that contains a QRS).

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Measuring Intervals:

I needed calipers to "solve" today's rhythm.

• PEARL #8: My favorite PEARL for distinguishing 2nd-degree from 3rd-degree AV block is knowing that in the presence of an underlying sinus rhythm — a QRS complex that occurs earlier-than-expected is probably conducted (therefore the rhythm is unlikely to be complete AV block!).
• In contrast — the escape rhythm with complete AV block will usually be regular (or at least, almost regular). This is why careful measurement of both PR and R-R intervals is essential for solving today's rhythm (See Figure-3).

Figure-3: I have carefully measured PR and R-R intervals.

Applying the Measurements in Figure-3:

• Note in Figure-3 that the ventricular rhythm is completely regular! (ie, all R-R intervals = 1680 msec.).
• Note also that despite "looking" similar — there is slight-but-definite variation in the PR interval from one beat to the next. This rules out the possibility of sinus rhythm with atrial bigeminy — because the PR interval varies from beat-to-beat (whereas it should be constant if the rhythm was sinus).
• As per PEARL #8 — None of the 6 beats in Figure-3 occur earlier-than-expected. This strongly suggests that none of the RED arrow P waves are being conducted — and that the rhythm probably is complete ( = 3rd-degree) AV block.
• As noted in PEARL #6 — despite marked variation in P wave morphology, I suspect that all RED arrow P waves are sinus impulses. In view of the likelihood of complete AV block — it would seem highly unlikely for the same pattern of P wave rhythmicity (ie, shorter-than-longer P-P intervals) — to be seen if the multiple variations in P wave shape were all originating from different atrial foci.
• 
  
• Advanced Point (Beyond-the-Core): Technically, the rhythm strip in today's tracing is too short to prove that the rhythm is complete AV block. This is because we do not see P waves occurring at all points within the R-R interval (ie, There are no P waves occurring near the middle of the R-R interval). That said, this does not matter clinically — because regardless of the degree of AV block, prompt referral to a PCI center is indicated given likely recent posterior OMI with marked bradycardia and at least 2nd-degree AV block.

LADDERGRAM:

I conclude my comments with a laddergram for the rhythm in today's case. At the least — there is no conduction of any of the RED arrow P waves because: i) The ventricular rhythm is regular (here, at a rate just under 40/minute); — and, ii) The PR interval continually varies.

• The QRS complex is narrow. This defines the escape rhythm focus as either arising in the AV node or from the Bundle of His (with the rate of less than 40/minute being a bit slow for an AV nodal escape rhythm).

Figure-4: My laddergram for today's case.

Take-Home POINTS:

• Today's case conveys a number of advanced concepts. My goal is to challenge experienced interpreters through discussion of these advanced concepts. As always — Your comments are welcome! 
• Recognition of the subtle ECG findings I point out regarding the 12-lead tracing in today's case are important details to be aware of! To Emphasize: As soon as I recognize significant bradycardia with some form of AV block — I actively look for recent evidence of acute OMI. By appreciating the need to look for subtle signs of recent inferior and/or posterior OMI — you greatly increase the chance that you will find it!
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• The above said — Today's case conveys important information for any level interpreter. Less experienced providers will hopefully appreciate how application of the Ps,Qs,3R approach allows you within seconds to recognize the essentials of today's rhythm enough to tell us to cancel non-emergent surgery, and to promptly refer this patient to a catheterization-capable center.

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Acknowledgment: My appreciation to Mohamed Salah (from Muscat, Oman) 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 #185 — Review of the Ps, Qs, 3R Approach for systematic rhythm interpretation.
• ECG Blog #188 — Reviews how to read and draw Laddergrams (with LINKS to more than 100 laddergram cases — many with step-by-step sequential illustration).

• ECG Blog #351 — reviews the diagnosis of acute posterior OMI. To see this illustrative case presented as an ECG Video — Please check out ECG Blog #406 (For a LINKED Contents to this ECG Video — Click on MORE in the Description under the video on YouTube).
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• ECG Blog #405 — ECG Video presentation that reviews the distinction between AV Dissociation vs Complete (3rd-degree) AV Block (For a LINKED Contents to this ECG Video — Click on MORE in the Description under the video on YouTube).
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• ECG Blog #164 — Which reviews step-by-step the diagnosis of a Mobitz I 2nd-degree AV block (with sequential laddergram illustration).
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• ECG Blog #258 — How to "Date" an Infarction based on the initial ECG.
• ECG Blog #294 — Reviews how to tell IF the "culprit" artery has reperfused.
• ECG Blog #230 — Reviews how to compare Serial ECGs.
• ECG Blog #115 — Shows how dramatic ST-T changes can occur in as short as an 8-minute period.
• ECG Blog #268 — Shows an example of reperfusion T waves.

• Diagnosis of an OMI from the initial ECG — Serial tracings with spontaneous reperfusion — then reocclusion! — See My Comment at the bottom of the page in the October 14, 2020 post on Dr. Smith's ECG Blog.
• Acute OMI that wasn’t accepted by the Attending — See My Comment at the bottom of the page in the November 21, 2020 post on Dr. Smith’s ECG Blog.
• Another overlooked OMI (Cardiologist limited by STEMI Definition — OMI evident by Mirror Test) — See My Comment at the bottom of the page in the September 21, 2020 post on Dr. Smith’s ECG Blog.
• Recognizing hyperacute T waves — patterns of leads — an OMI (though not a STEMI) — See My Comment at the bottom of the page in the November 8, 2020 post on Dr. Smith's ECG Blog.

ADDENDUM (1/20/2024): 

• Included below is a series of additional material relevant to today's case. 

 

Free PDF Downloads from relevant Sections in my ECG-2014-ePub:

• PDF File: Overview on the Cardiac Circulation and the “Culprit” Artery in Acute MI —
• PDF File: Posterior MI and the “Mirror Test” —

 

Figure-5: ECG findings to look for when your patient with new-onset cardiac symptoms does not manifest STEMI-criteria ST elevation on ECG. For more on this subject — SEE the September 3, 2020 post in Dr. Smith’s ECG Blog with 20-minute video talk by Dr. Meyers on The OMI Manifesto. For my clarifying Figure illustrating T-QRS-D (2nd bullet) — See My Comment at the bottom of the page in Dr. Smith’s November 14, 2019 post.

 

Figure-6: KEY points in the recognition of isolated posterior MI (This figure is taken from ECG Blog #193 — in which I review the "Basics" for predicting the "culprit" artery). 

—  — 

ECG Media PEARL #60 (8:30 minutes Audio) — Reviews use of the "Mirror Test" to facilitate recognition of: i) Acute Posterior MI; ii) Acute High-Lateral or Inferior MI (ie, the "magical" reciprocal relationship between leads III and aVL); and, iii) Anterior ST elevation due to LVH (that is not indicative of anterior MI).

 

—  —

ECG Media PEARL #10 (10 minutes Audio) — reviews the concept of why the term “OMI” ( = Occlusion-based MI) should replace the more familiar term STEMI — and — reviews the basics on how to predict the "culprit" artery.

—  —

ECG Media PEARL #11 (6 minutes Audio) — Reviews how to tell IF the “culprit” (ie, acutely occluded) artery has reperfused, using clinical and ECG criteria.

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Additional Material on Today's CASE:

—  —

ECG Media PEARL #4 (4:30 minutes Audio): — takes a brief look at the AV Blocks — and focuses on WHEN to suspect Mobitz I.

ECG Media Pearl #8 (8:20 minutes Video) — ECG Blog #191 — Distinguishing between AV Dissociation vs Complete AV Block (2/6/2021).

ECG Media Pearl #9 (5:40 minutes Video) — ECG Blog #192 — Reviews the 3 Causes of AV Dissociation (2/9/2021).

• 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). 

ECG Blog #412 — Is Cardiac Cath Indicated?

The ECG in Figure-1 was obtained from a middle-aged man with known hypertension — who presented to the ED (Emergency Department) for CP (Chest Pain) over the preceding 2-3 days.

QUESTIONS:

• How would YOU interpret the ECG in Figure-1?
• Should you activate the cath lab?  If not — What next? 

Figure-1: The initial ECG in today's case — obtained from a middle-aged man with CP for the past 2-3 days. To activate the cath lab?

The Initial ECG in Today’s CASE:

The rhythm in ECG #1 is sinus at 65-70/minute. Intervals (PR - QRS - QTc) are all within normal limits. The axis is slightly leftward (at about -10 degrees — as suggested by slight negativity of the small amplitude QRS in lead aVF — but not negative enough to qualify as LAHB, because the QRS in lead II is all positive).

• Voltage for LVH is easily satisfied in many leads (Very tall R wave in lead I — R in lead aVL ~20 mm [given overlap with the S wave in lead aVR] — deep S waves in V1,V2 + tall R waves in V5,V6 ≥35 mm). 
• For more regarding ECG criteria for LVH — See the ADDENDUM below and/or ECG Blog #73 and ECG Blog #245.

Regarding Q-R-S-T Changes:

• Q Waves — Tiny normal septal q waves in leads I,aVL.
• R Wave Progression — Normal R wave progression — with appropriate transition (where the R wave becomes taller than the S wave is deep) occurring between leads V3-to-V4.
• ST-T Wave Changes — There is ~1 mm of lateral J-point ST depression, with coving of ST segments and deep symmetric T wave inversion (seen in leads I,aVL; V4,5,6). There is 1-2 mm of ST elevation in leads III,aVF and V1 — with the T waves in leads III and aVF being disproportionately tall and "bulky" (with a mirror-image opposite appearance to the J-point depression and deep T wave inversion seen in lateral leads). 

MY Impression of ECG #1:

As a single tracing in a patient with 2-3 days of CP — this is a difficult ECG to interpret. My thoughts were as follows:

• The rhythm is sinus. Marked LVH is suggested by greatly increased QRS amplitude in multiple leads in this patient with longstanding hypertension (See Figure-3 in the ADDENDUM below for the ECG criteria for LVH that I favor).
• My written interpretation on a tracing such as this one would read, "Marked LVH and 'strain' and/or ischemia — with need for clinical correlation." 
• Pure LV "strain" tends to produce downsloping ST depression with asymmetric T inversion in ≥1 of the lateral leads (ie, leads I,aVL; V5,V6). Although it is not uncommon in patients with marked hypertension to see deep, symmetric T wave inversion in lateral leads — pure LV "strain" is generally not associated with ST coving, as is clearly seen in lead V4 of ECG #1 (See Figure-4 below in the ADDENDUM for the ECG picture of typical LV "strain" ).
• In addition — the ST elevation in leads III and aVF, in association with the hypervoluminous T waves in these leads — is not expected with pure LV "strain".
• On the other hand — the ST elevation seen in lead V1 is perfectly consistent with LVH and LV "strain" (ie, The shape of this ST-T wave in lead V1, in association with the deep S wave in this lead — is a mirror-image opposite picture of the typical expected appearance of LVH with "strain" in a lateral chest lead).
• 
  
• BOTTOM Line: Today's patient presented with a 2-3 day history of chest pain and the ECG shown in Figure-1. While this initial ECG is not diagnostic of an OMI (ie, of acute coronary Occlusion) — there are enough findings present in ECG #1 that are not expected with simple LVH and "strain", such that further evaluation is clearly indicated.

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The CASE Continues:

The first 2 high-sensitivity troponin values returned slightly elevated. A prior ECG from 9 years earlier was found. For ease of comparison — I have put this patient's baseline tracing and his initial ECG in today's case together in Figure-2.

• Does seeing this patient's "baseline" ECG change your interpretation of ECG-1?

Figure-2: Comparison of the 2 ECGs in today's case.

Comparison of the 2 ECGs in Figure-2:

Availability of a prior tracing on today's patient confirms that all of the ST-T wave abnormalities described above for ECG #1 — are new compared to this patient's baseline tracing done 9 years earlier.

• Limb lead QRS amplitudes have greatly increased since the ECG baseline done 9 years earlier.
• Given the large amplitude of the QRS complex in lead V2 of ECG #2 — I found it hard to determine if overall chest lead amplitude was changed.
• There was no ST elevation and no hypervoluminous T waves in leads III and aVF of ECG #2 that was done 9 years earlier.
• There was no J-point depression — no ST segment coving — and no T wave inversion on the prior ECG.
• 
  
• BOTTOM LINE: ECG changes of LV "strain" and/or ischemia that we see on today's initial ECG — were not present 9 years earlier. That said — We have no idea when during this 9-year interim period these abnormal ST-T wave findings may have developed.

CASE Follow-Up:

In view of this patient's CP at the time he was seen in the ED — the 2 slightly elevated troponin values — and the abnormal ST-T wave findings on the initial ECG (with all of these ST-T wave changes being new since the baseline ECG done 9 years earlier) — Cardiac cath was performed.

• Cardiac cath showed normal coronary arteries.
• Cath pictures and the formal Echocardiogram indicated apical HCM (Hypertrophic CardioMyopathy) as the probable etiology of the abnormal ECG in Figure-1.

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COMMENT:

To emphasize —  Cardiac catheterization was completely appropriate in today's case — as today's patient presented with ongoing CP over the 2-3 days before he arrived in the ED — troponin was elevated (albeit modestly) — and his initial ECG did show ST-T wave changes that suggested "something more" than simple LVH (albeit not being overly suggestive of acute coronary occlusion).

• Taking another LOOK at today's initial ECG (and secure with the knowledge from cardiac catheterization that today's patient does not have an acute OMI [ = Occlusion-based MI] — but instead has apical HCM) — the ECG in Figure-1 is completely consistent with this diagnosis! 
• ST-T wave changes in Figure-1 are localized to lateral leads (ie, leads I,aVL; and V4,5,6) — especially in leads with increased QRS amplitude. In contrast — with LAD occlusion, there is usually at least modest associated ST elevation in lead aVL (and often also in lead I).
• There is no loss of R wave in anterior leads in Figure-1 (as opposed to poor R wave progression that is commonly seen with LAD OMI).
• The ST-T wave picture in lead V1 of Figure-1 is typical of LVH with "strain" (ie, It is the mirror-image opposite picture of what lateral chest leads typically show with marked LVH).
• Rather than Wellens' T waves — the most abnormal appearing chest lead ( = lead V4) is much more suggestive of a transitional (repolarization) change from the positive ST-T waves in leads V1,2,3 — "on the way" to ST coving and deep T wave inversion seen in the remaining chest leads. Like recognition of a face that you know, but have trouble describing in words — this appearance does not suggest OMI.
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• P.S.: An additional reason justifying prompt cardiac cath in today's case — is how different the initial ECG in Figure-1 looked compared to the "baseline" ECG on file. It would be interesting to see what an Echo from 9 years earlier looked like — but we do not know if such a study was previously done. It therefore appears that this patient's apical HCM continued to evolve over this 9 year period (rendering it impossible to be certain that ST-T wave abnormalities in Figure-1 were all attributable to apical HCM and not acute ischemia).

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About HCM (Different Forms of this Entity):

I've excerpted what appears below from My Comment in the December 26, 2023 post in Dr. Smith's ECG Blog.

HCM is an "umbrella term" applied to the presence of LVH in the absence of "abnormal cardiac loading conditions" (Hughes et al — JAHA 9:e015294, 2020). These are often felt to be the result of autosomal dominant mutations in sarcomeric protein genes — and may present with a number of distinct LVH forms, including the "classic" = asymmetric septal hypertrophy form (which is the type most commonly referred to when the abbreviation "HCM" is used) — concentric HCM — reverse septal — neutral — and apical HCM (initially known as Yamaguchi Cardiomyopathy — and sometimes abbreviated as ApHCM ).

• Clinically — Overall management of the above different morphological forms of HCM is similar for the emergency provider. That said — distinction between "classic" HCM vs the apical HCM form may be useful because: i) ECG findings tend to be different (Lyon et al — Europace 20:102-112iii, 2018); — ii) Echo appearance is different when hypertrophy localizes to the apex; and, iii) There is a significantly greater incidence of AFib with apical HCM.
• 
  
• Beyond the scope of this ECG Blog — specific formal Echo findings may help to sort through the large "spectrum" of HCM disorders — encompassing "lower risk" HCM (in those with modest or moderate hypertrophy — but without obstruction) — vs higher-risk obstructrive forms of HCM.

ECG Findings with HCM:

Most patients with HCM do not have a normal ECG. Among the many ECG findings that may be seen in patients with "classic" HCM are the following:

• Increases in QRS amplitude.
• Large septal Q waves (Sometimes known as "dagger" Q waves — because these are deep but narrow Q waves seen in lateral leads). 
• Tall R wave in lead V1 and/or early transition in the chest leads (reflecting increased "septal" forces).
• Abnormal ST-T wave abnormalities.
• Conduction defects (ie, LBBB, IVCD).
• WPW 
• Cardiac arrhythmias (including AFib). 
• 
  
• The Problem: None of the above ECG findings are specific for HCM. The variety of potential ECG findings with "classic" HCM is great — which poses problems when contemplating whether or not to use the ECG as a screening tool in athletes.

ECG Findings with Apical HCM:

Apical HCM makes up a minority of patients who qualify as having "HCM" (ie, less than 10% in the non-Asian population). 

• With the exception "dagger" Q waves (which are typically a result of a thickened septum) — any of the other ECG findings listed above for "classic" HCM may be seen with apical HCM.
• The ECG finding that is most characteristic of apical HCM is the presence of Giant T waves. Although T wave inversion in ECG #1 is prominent — it is not quite deep enough to qualify as true "Giant" T waves (See ECG Blog #276 and ECG Blog #309).

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NOTE: For more on HCM, with a summarizing Table on the treatment approach to this group of disorders — Please check out My Comment in the October 28, 2023 post in Dr. Smith's ECG Blog.

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Acknowledgment: My appreciation to 林柏志 (from Taiwan) 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 (outlined in Figures-2 and -3, and the subject of Audio Pearl MP-23 in Blog #205).
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• ECG Blog #209 — and ECG Blog #254 — Reviews a case of marked LVH that results in similar ST-T wave changes as may be seen with Wellens' Syndrome.
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• ECG Blog #245 — Reviews the ECG diagnosis of LVH.
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• ECG Blog #276 — and ECG Blog #309 — Reviews the entity of Giant T waves.

• 
  
• ECG Blog #73 — Reviews "My Take" on the ECG Diagnosis of LVH. 
• ECG Blog #92 — Presents another perspective for ECG Diagnosis of LVH.
•  
• The November 4, 2018 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) reviews 3 ECG Clues for rapid recognition of erroneous lead V1,V2 placement. 
• The March 31, 2019 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) illustrates the potentially misleading effect the pre-hospital ECG may have in patients with LVH, by cutting off S wave voltage in the anterior leads. 
• The March 29, 2019 post in Dr. Smith's ECG Blog — My Comment regarding Tracing A (at the bottom of the page) illustrates how LVH is a common mimic of acute ischemia. 
• The December 27, 2018 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) illustrates a case with anterior ST elevation from LVH that may falsely suggest acute anterior infarction.

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ADDENDUM (1/13/2024):

I've added below in Figure-3 and Figure-4 additional material to facilitate ECG diagnosis of LVH and LV "strain".

 

—  —

ECG Media PEARL #59 (9:10 minutes Audio) — Reviews the ECG diagnosis of LVH (and its impact clinically with both chronic and acute cardiac disorders).

Figure-3: The voltage and other criteria I favor for ECG diagnosis of LVH (Please see ECG Blog #73 for additional details).

Figure-4: ST-T wave appearance of normal (A) — vs "strain" (C) or a strain "equivalent" pattern (B) — vs ischemia (D). (Please see ECG Blog #73 for additional details).