Saturday, February 10, 2024

ECG Blog #416 — Is the Rhythm and ECG related?


Imagine the only information provided for the ECG in Figure-1 — is that it was obtained from a 60-year old man with new CP (Chest Pain).


QUESTIONS:
  • In view of this brief history — How would YOU interpret this ECG in Figure-1?
  • Is the cardiac rhythm related to the 12-lead ECG?

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

MY Thoughts on the ECG in Figure-1:
The goal of practicing clinicians is to interpret both parts of the tracing in Figure-1 ( = the cardiac rhythm and the 12-lead ECG) — in an optimal time-efficient manner. 
  • To accomplish the above goal — our interpretation of these 2 Parts of today’s tracing need not necessarily be complete on our initial assessment. 
  • Instead — in an acute case such as today’s (ie, in which the patient presents for new CP) — I favor spending no more than 5-to-10 seconds looking at the rhythm (to ensure that no immediate treatment is needed for this rhythm). 
  • I then turn my attention to the 12-lead ECG to assess whether an acute OMI is likely to be present (in order to quickly determine IF prompt cardiac cath and potential PCI might be needed).

  • PEARL #1: Although I favor limiting the amount of time spent assessing today’s complex rhythm to no more than 5-to-10 seconds — I still favor using the systematic Ps, Qs, 3R Approach (See ECG Blog #185) because: i) With minimal practice — you’ll find this systematic approach actually speeds up your assessment, rather than slowing it down; and, ii) Your accuracy in interpretation will improve (such that even if you do not arrive at a definitive diagnosis — you will limit diagnostic possibilities).
 

My Quick Assessment of Today’s Rhythm:
By the Ps, Qs, 3R Approach:
  • The rhythm in Figure-1 is clearly not Regular. That said — it is supraventricular (because the QRS complex is not wide). The overall Rate is slow, dropping in places to less than 50/minute. P waves are present — but the PR interval appears to be continually changing (ie, which raises the question as to whether any of the P waves are Related to neighboring QRS complexes?).

  • To EMPHASIZE: The above targeted assessment by the Ps,Qs,3R Approach should not take more than 10-20 seconds. This is all the information that you need for an initial Quick Assessment of the cardiac rhythm. 
  • NOTE: Although the rate of the rhythm is quite slow in places — IF the patient is hemodynamically stable, then there is no emergent treatment needed (ie, There is no immediate need for a more precise interpretation of the rhythm). This means that you can now turn your attention to the 12-lead ECG to determine IF prompt cath is (or is not) immediately needed in this patient with new CP.

PEARL #2:
 Looking first at the cardiac rhythm — I was not initially sure IF some form of 2nd-degree AV block might be present. That said — I instantly knew that today’s rhythm was unlikely to be complete AV block because the ventricular response is so irregular! 
  • Most of the time when there is complete (3rd-degree) AV block — the ventricular response will be regular (or at least almost regular). This is beause IF none of the P waves are able to conduct to the ventricles (as would be the case if complete AV block was present) — a regular escape focus (either from the AV Node or from the ventricles) will usually take over the rhythm. The marked irregularity seen in Figure-1 is simply too variable to arise from a normally functioning escape focus.

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Turning Attention to the 12-Lead ECG:
At this point in our interpretation — We need to focus on the 12-lead ECG. I've highlighted in Figure-2 the KEY leads that should capture your attention. In sequence, over the next 20-to-30 seconds — your eye should focus on the complexes within the RED — then light BLUE — then dark BLUE rectangles.
  • In this patient with new CP — What do YOU now know?
  • What intervention is needed?
  • What does this tell us about the likely etiology of the rhythm?

Figure-2: I've highlighted the KEY complexes in the 12-lead ECG.


Interpretation of Today’s 12-Lead ECG:
In view of the history of new CP — YOUR assessment of the 12-lead ECG in Figure-2 should acknowledge the following:
  • Within the RED rectangle: — The "shelf-like" flat ST segment with abrupt angulation into a prominent upright T wave in lead V2 is immediately diagnostic of acute posterior OMI (where the “O” in “OMI” indicates an acute MI that is due to acute coronary Occlusion). 
  • KEY Clinical Point: Normally, there should be gentle upsloping of a slightly elevated ST segment in leads V2 and V3 — such that our "eye" should immediately recognize the abnormal shape of the complex within the RED rectangle (that tells us “posterior OMI” until proven otherwise). 

  • Within the 3 light BLUE rectangles: — Because of their common blood supply, posterior OMI is regularly associated with inferior OMI. Consequently — confirmation that the abnormal shape of the ST-T wave in lead V2 is truly the result of acute posterior OMI will be forthcoming IF limb leads are diagnostic of acute inferior MI. Note within each of the light BLUE rectangles — that there are small-but-real Q waves with subtle-but-real ST elevation. Especially in view of the modest QRS amplitudes — the ST-T wave in lead III clearly looks hyperacute (ie, disproportionately "fatter"-at-its-peak and wider-at-its-base than it should be — with subtle terminal negativity of the T wave).

  • Within the dark BLUE rectangle: — The "magical" mirror-image opposite ST-T wave picture in lead aVL to that seen in lead III removes all doubt. Given tiny amplitude of the QRS in lead aVL — the disproportionate area within the depressed ST segment in this lead is a reciprocal change that confirms acute inferior OMI (Note terminal T wave positivity in lead aVL — that also reflects the mirror-image of the subtle terminal T wave negativity in lead III).

  • BOTTOM Line: In less than a minute — We can confirm that in today’s patient, who presents for evaluation with new CP — the ECG in Figure-2 is diagnostic until proven otherwise, of acute infero-postero OMI (most likely from acute RCA occlusion). Prompt cath for PCI is clearly indicated!

  • PEARL #3: An advanced clinical concept — is that acute inferior MI is commonly associated with 2nd-degree AV blocks of the Wenckebach (Mobitz I) type. Awareness of this common association made me instantly suspect that some type of Wenckebach conduction is probably operative in today's rhythm — even though I admittedly do not see any pattern of consistent group beating, or any repetitive PR intervals that typically clue me in to Mobitz I conduction defects.
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A Closer Look at Today's Rhythm:
To Emphasize: The important "Take Home" Message from today's case — is that in this patient with new CP — the ECG in Figure-2 is diagnostic of acute infero-postero OMI (most likely from acute RCA occlusion) — and that prompt cath for PCI is needed.
  • Whatever the specific etiology of today's arrhythmia is, the “good news” is — that this rhythm will most probably improve with reperfusion of the "culprit" artery.

  • That said — I found today's arrhythmia fascinating, and worthy of more in-depth analysis. (NOTE: The laddergram solution I propose below for today’s rhythm is complex and clearly Beyond-the-Core. That said — I believe my description and step-by-step construction of the laddergram below should prove insightful to any level provider.). 

  • As a reminder — learning to draw laddergrams does take some time and is not needed to become experienced and skilled in clinical arrhythmia interpretation. But — learning how to read laddergrams that are already drawn is EASY — and all clinicians (regardless of their level of experience) can quickly begin to benefit from the insight provided by laddergram illustration.
  • For readers with an interest in learning either how to read and/or draw laddergrams — I have added LINKS to more than 100 laddergrams (many with step-by-step illustration) at this site = https://tinyurl.com/KG-Laddergrams —
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How to Proceed for “Solving” Today’s Arrhythmia:
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PEARL #4: At this point — Label the P waves!
  • The simple step of labeling P waves is tremendously helpful in visualizing potential relationships between atrial activity and neighboring QRS complexes.
  • Using calipers facilitates the process. I simply set my calipers at a P-P interval determined by selecting the distance between 2 P waves that I can identify with certainty. Because "ventriculophasic" sinus arrhythmia is so commonly seen with 2nd- and 3rd-degree AV blocks — We need to factor in the reality that the P-P interval between sinus P waves will often vary slightly.

Take a LOOK at Figure-3 — in which I've labeled sinus P waves with RED arrows throughout the rhythm strip.
  • Are any PR intervals the same?
  • Do you think any of the QRS complexes in Figure-3 are being conducted? If so — How can you tell that P waves are conducting these QRS complexes?

Figure-3: I've labeled P waves with RED arrows.


MY Thoughts on Figure-3:
  • RED arrows highlight a fairly regular atrial rhythm (with slight variation in the P-P interval due to ventriculophasic sinus arrhythmia).
  • As noted earlier in PEARL #2 — today’s rhythm is unlikely to represent complete AV block. This is because of the marked irregularity of the ventricular rhythm (whereas complete AV block most often manifests a regular, or at least fairly regular ventricular rhythm).
  • Most R-R intervals in the long lead II rhythm strip contain 2 P waves between QRS complexes — which means that at least 1 of these P waves is not conducted. This strongly suggests that the irregular rhythm in Figure-3 represents some form of 2nd-degree AV block (ie, either Mobitz I [ = AV Wenckebach] or Mobitz II).
  • IF this is true — then the fact that the QRS complex is narrow everywhere — that the PR interval is not constant — and, that the 12-lead ECG is diagnostic of an acute infero-postero OMI — suggests some form of 2nd-degree AV Wenckebach is operative (because with Mobitz II — the PR interval is constant for consecutively conducted beats — the QRS is almost always wide, and anterior rather than inferior infarction has occurred).
  • BUT — If the rhythm in Figure-3 indeed represents some form of AV Wenckebach — it is not a "typical" form of AV Wenckebach, because there is no consistent pattern of group beating — and, similar PR intervals are lacking, whereas they are commonly seen with this Mobitz I form of 2nd-degree AV block. Instead — the PR interval in front of each of the 9 beats in today's tracing is constantly changing — which raises the question as to whether any of the P waves are being conducted to the ventricles?


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The LADDERGRAM: 
At this point I needed a laddergram to help me work out what might be a plausible mechanism for today's complex arrhythmia.
  • NOTE: As I've commented on in a number of previous blog posts — Wenckebach conduction may occur at more than a single level within the AV Node. When this happens — complex conduction relationships may be seen, including non-conduction of consecutive on-time P waves (See ECG Blog #259 for more on Dual-Level AV Wenckebach — which is what I suspected in today's complex rhythm in which the PR interval constantly changes — and, in which 2 P waves are contained within most R-R intervals).
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Figure-4: Laddergram STEP-1. It is usually easiest to begin a laddergram by filling in the Atrial Tier. BLUE arrows show the onset of P waves as my reference point for drawing in atrial activity. Because conduction through the atria is generally rapid — I drew in near-vertical lines in the Atrial Tier.

NOTE:
 Because I suspected dual-level AV block within the AV Node — I divided the AV Nodal Tier into 2 parts by drawing in a horizontal BLACK dotted line).



Figure-5: Laddergram STEP-2. I next fill in the Ventricular Tier. BLUE arrows show the onset of each QRS complex as my reference point for each of the 9 supraventricular beats in this tracing. Once again, since conduction of narrow-QRS beats through the ventricles is generally rapid — I drew in near-vertical lines for each of the 9 narrow QRS beats in the Ventricular Tier.


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NOTE: The "EASY part" for constructing most laddergrams consists of these first 2 STEPS (that are shown in Figure-4 and Figure-5). 
  • Now the challenge begins! — with the task of trying to figure out which of the P waves in the Atrial Tier are being conducted to the ventricles.

  • PEARL #5: The BEST clue that a P wave is conducting a QRS complex to the ventricles — is when, in association with an underlying sinus rhythm (ie, in which there are no PACs or PJCs) — you see a QRS complex that clearly occurs earlier-than-expected. This concept is best illustrated in Figure-6.
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Figure-6: Of the 9 beats in Figure-6 — The QRS complex that most clearly occurs earlier-than-expected is beat #8. By PEARL #5 — this suggests that beat #8 is a QRS complex that is being conducted to the ventricles. Since beat #8 is neither a PAC nor PJC (because the underlying sinus rhythm remains quite regular — and a PAC or PJC would have reset the underlying sinus rhythm) — it must be that P wave "n" is conducting beat #8, albeit with a markedly prolonged PR interval (represented by the dark BLUE lines that pass through the 2 levels within the AV Nodal Tier).  

P wave "o", which falls right at the beginning of beat #8 — has too short of a PR interval to conduct (as I have represented by the light BLUE butt end that shows non-conduction of this impulse).




Figure-7: I fully acknowledge that because of the complexity of today's arrhythmia — some "Trial and Error" was needed along my way toward drafting the most logical solution to the laddergram for today's rhythm.

The position of P wave "l" (occurring so soon after the previous QRS complex) — seemed extremely unlikely to be conducting beat #7. This is especially true because P wave "m" appears in a much better position to conduct beat #7. I therefore drew in a light BLUE butt end to indicate non-conduction of P wave "l" — and dark BLUE lines that pass through the 2 levels within the AV Nodal Tier to indicate conduction of P wave "m". Note that the incline of the RED line within the lower AV Nodal Tier is greater than the incline of the dark BLUE line — consistent with a PR interval that is increasing until P wave "o" is non-conducted. (This makes for 3:2 AV Wenckebach conduction cycle within the AV Nodal Tier).




Figure-8: I next looked at P waves "p" and "q". One of these 2 P waves will most probably be conducting beat #9 to the ventricles. Because P wave "q" seems much better positioned to be conducting (ie, with a slightly, but not excessively prolonged PR interval) — I felt reasonably sure that P wave "p" was not conducting. This meant that 2 P waves in a row (P waves "o" and "p") were not conducting. This finding supported my suspicion of dual-level AV block within the AV Node, as the most logical explanation for there to be consecutive non-conducted P waves in a 2nd-degree AV block that is not Mobitz II. (I show this non-conduction of P waves "o" and "p" by successive butt end RED lines at each of the 2 levels within the AV Nodal Tier).




Figure-9: I next turned my attention to P waves "j" and "k". Once again, it seems logical that 1 of these 2 P waves will probably be conducting beat #6 to the ventricles. And once again, because P wave "k" seems much better positioned to be conducting (ie, with a slightly, but not excessively prolonged PR interval) — I felt reasonably sure that P wave "j" was not conducting. (This makes for a 2:1 AV conduction cycle — presumably by association being a 2:1 AV Wenckebach cycle).




Figure-10: At this point — a pattern for conduction of atrial impulses seemed to be established. By assessing atrial activity within each R-R interval — it became easier to intuit which P waves seemed least likely to be conducting — therefore suggesting that the remaining P wave(s) were indeed conducting neighboring QRS complexes to the ventricles.

P wave "i" seems perfectly positioned to conduct beat #5 to the ventricles (in a similar way that P waves "k" and "m" seemed well positioned to be conducting beat #6 and beat #7, respectively). IF this assumption is correct — then P waves "g" and "h" are not conducting any QRS complex to the ventricles. As was the case for P waves "o" and "p" — this makes for 2 non-conducted P waves in a row (which is why I drew successive butt end BLUE lines for P waves "g" and "h" at each of the 2 levels within the AV Nodal Tier).

Working my way backward — I next noticed how much earlier-than-expected beat #3 occurs, which as per PEARL #5 — strongly suggests that beat #3 is being conducted to the ventricles. But the PR interval of P wave "e" until neighboring beat #3 is clearly too short to conduct! Therefore, it must be that P wave "d" is conducting beat #3, albeit with a very long PR interval (in the same way we deduced that P wave "n" is conducting beat #8 with a long PR interval).

This left me with P waves "b" and "c" — which given the "pattern" of conduction observed up to this point, rendered it EASY for me to postulate that P wave "c" was much better positioned for conducting its neighboring QRS complex ( = beat #2) than P wave "b".

Finally — There is P wave "a" and beat #1. Although impossible to know for certain (because we do not see what happens before beat #1) — I drew in what seems to be the most logical conduction for this first part of today's rhythm (The PR interval between P wave "a" and beat #1 clearly seems too short to conduct).




Figure-11: My "finished" laddergram. Note that despite the lack of similar groups of beats that repeat (and the lack of repetitive PR intervals) — STEPPING BACK from Figure-11 does illustrate the concept of dual-level AV Wenckebach, in which there is progressive lengthening of PR intervals (represented by progressive increase in angulation within each of the 2 AV Nodal levels) — until 1 or 2 P waves in a row are dropped — with typical Wenckebach periodicity beginning again after the brief pause.



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Final COMMENT: 
Today's rhythm is difficult to interpret! That said — there are important lessons to be learned from review of today’s case.
  • Precise determination of the etiology of today's arrhythmia is not needed for optimal initial management of today's patient! Instead — my Quick Assessment of the rhythm (which should not take more than 10-20 seconds to complete) is all that is needed for optimal initial management of today's patient.
  • The KEY finding in today's ECG — is recognition in this patient with new CP that the tracing in Figure-2 is diagnostic of acute infero-postero OMI — and that prompt cath is needed for PCI.
  • Whatever today's rhythm turns out to be — the "good news" is that the bradycardia and degree of AV block is likely to improve as soon as there is reperfusion of the "culprit" artery (Therefore need for prompt cath with PCI).

  • Being able to draw a laddergram of today's complex arrhythmia is not essential for optimal initial management of today's patient. That said — it is good to be aware of the entity known as dual-level AV Wenckebach as a less common, but nevertheless important form of 2nd-degree AV block. My hope is that review of my step-by-step approach to solving today's arrhythmia proves insightful for suggesting when dual-level AV Wenckebach should be suspected.
  • Learning to read laddergrams that are drawn is EASY. Hopefully my step-by-step laddergram approach increases appreciation of the Wenckebach conduction pattern occurring in today's rhythm that is not otherwise obvious.

  • Finally — I will emphasize that my finished laddergram in Figure-11 is not the only possible solution to today's arrhythmia. More than a single solution is possible for many complex arrhythmias. What counts — is that my laddergram is a possible solution — and that some form of 2nd-degree AV block with periods of Wenckebach conduction is present.


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Acknowledgment: My appreciation to Adem Med Ahmed (from Mauritania) and Ahmed Elbakery (from Yemen) 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 — Reviews my System for Rhythm Interpretation, using the Ps, Qs, 3R Approach.
  • ECG Blog #188 — Reviews how to read and draw Laddegrams (with LINKS to more than 100 laddergram cases — many with step-by-step sequential illustration).

  • ECG Blog #192 — The 3 Causes of AV Dissociation.
  • ECG Blog #191 — Reviews the difference between AV Dissociation vs Complete AV Block.

  • ECG Blog #389 — ECG Blog #373 — and ECG Blog #344 — for review of some cases that illustrate "AV block problem-solving".
  • ECG Blog #251 — Reviews the concepts of Wenckebach periodicity and the "Footprints" of Wenckebach.
  • ECG Blog #164 — Reviews a case of typical Mobitz I 2nd-Degree AV Block (with detailed discussion of the "Footprints" of Wenckebach). 

  • ECG Blog #63 — Mobitz I, 2nd-Degree AV Block with Junctional Escape Beats.
  • ECG Blog #267 — Reviews with step-by-step laddergrams, the derivation of a case of Mobitz I with more than a single possible explanation.

  • ECG Blog #259 — Reviews step-by-step laddergram for a patient with Dual-Level AV Block.
  • ECG Blog #243 — Reviews a case of AFlutter with Dual-Level Wenckebach out of the AV Node.
  • ECG Blog #226 — Works through a complex Case Study (including an 11:00 minute ECG Video Pearl that walks you through step-by-step in the construction of a laddergram with Wenckebach conduction and dual-level block within the AV node).
  • ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
  • ECG Blog #218 — Reviews HOW to define a T wave as being Hyperacute? 

  • ECG Blog #193 — 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 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).

  • 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).



 
ADDENDUM (2/10/2024):



This 15-minute ECG Video (Media PEARL #52) — 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.




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

  • Section 2F (6 pages = the "short" Answer) from my ECG-2014 Pocket Brain book provides quick written review of the AV Blocks.
  • 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!



ECG Media PEARL #71 (5:45 minutes Audio) — Reviews the phenomenon of Dual-Level Wenckebach out of the AV Node (HOW to recognize this phenomenon — and how to distinguish it from Mobitz II).



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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-12: 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.




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.


 










Sunday, February 4, 2024

ECG Blog #415 — The Cath showed NO Occlusion!


Today’s patient is an older woman who experienced a number of fainting epiodes over the previous week. No CP (Chest Pain). Shortly after arrival in the ED (Emergency Department) — she suffered a cardiac arrest. The ECG in Figure-1 was obtained following successful resuscitation.
  • Stat Echo — obtained shortly after successful resuscitation revealed anterior wall akinesis.
  • BUT — Cardiac catheterization done a little later did not reveal any significant stenosis.


QUESTIONS:
  • In view of the above history — How would YOU interpret the ECG in Figure-1?
  • How can you explain that no “culprit” artery was found on cardiac catheterization?
  • What is T-QRS-D? Is this ECG finding present in today’s initial ECG? 

Figure-1: The initial ECG in today's case — obtained after successful resuscitation from cardiac arrest. (To improve visualization — I've digitized the original ECG using PMcardio).


MY Thoughts on Today’s CASE:
Fortunately — Today’s patient was successfully resuscitated following her cardiac arrest. Despite the absence of significant coronary stenosis on her post-arrest cath — the ECG in Figure-1 is clearly diagnostic of an extensive anterolateral STEMI (presumably from acute LAD [Left Anterior Descending] coronary artery occlusion).
  • The rhythm in ECG #1 is regular and supraventricular at a rate of ~75/minute. Although I do not clearly see sinus P waves in lead II (ie, only the 1st beat seems to have an upright P wave in lead II) — the QRS complex is narrow in all 12 leads, and a small, upright P wave with fixed PR interval is seen in lead V1 (RED arrows in Figure-2).
  • There is marked LAD (Left Axis Deviation) — with predominant negativity in lead II, consistent with LAHB (Left Anterior HemiBlock).
  • No chamber enlargement.

Regarding Q-R-S-T Changes:
  • Q Waves — A very small, but somewhat widened Q wave of uncertain significance is seen in lead aVL. Tiny-but-present initial R waves are seen in each of the inferior leads (consistent with LAHB — but not indicative of inferior infarction).
  • R Wave Progression — Although an initial R wave is seen in anterior leads V1,V2,V3 — there is loss of R wave amplitude between lead V1-to-V2.
  • ST-T Wave Changes — The most dramatic change is the marked ST elevation that begins in lead V2 — and which remains substantial throughout the rest of the precordial leads. T waves in the inferior leads look more-peaked-than-expected given QRS amplitude in these leads — and there is reciprocal ST-T wave depression in lead aVL.
  • There is T-QRS-D (Terminal QRS Distortion) in leads V4,V5,V6 (BLUE arrows in Figure-2) — as discussed in detail below).

IMPRESSION of Today’s ECG:
As emphasized above — the post-arrest ECG in Figure-2 is clearly diagnostic of an extensive anterolateral STEMI.
  • As best we can tell from the history we are given — this patient had syncope but no CP prior to her acute event. As discussed in detail in ECG Blog #228 — this seemingly qualifies as a “Silent” MI (Approximately half of those MIs not accompanied by CP — have some other associated symptom such as syncope, which substitutes as a “chest pain equivalent”).
  • The fact that cardiac cath performed shortly after cardiopulmonary resuscitation failed to reveal any significant coronary stenosis (ie, No evidence of any “culprit” artery) — qualifies today's case as MINOCA ( = MI with Non-Obstructive Coronary Arteries — which I discuss in detail below).


Figure-2: I've labeled sinus P waves in lead V1 — and T-QRS-D in leads V4,V5.



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What is T-QRS-D?
The concept of Terminal QRS Distortion (T-QRS-D) was unknown to me prior to becoming an Associate Editor in Dr. Smith's ECG Blog. Since then I've seen many clinical cases that validate this ECG finding promoted by Dr. Stephen Smith.
  • T-QRS-D — is defined as the absence of both a J-wave and an S-wave in lead V2 — and/or lead V3 — and/or lead V4 (T-QRS-D may be seen in leads other than V2,V3,V4 — but its clinical significance when T-QRS-D is only seen in other leads is less certain). 
  • NOTE: T-QRS-D is simple to define. That said — this ECG finding may be subtle! I fully acknowledge that it has taken me some time to become comfortable and confident in its recognition.

  • Clinical Significance: When present — T-QRS-D may provide invaluable assistance for distinguishing between a repolarization variant vs acute OMI. When true T-QRS-D is present in a patient with new symptoms — it is virtually diagnostic of acute OMI ( = of an acute coronary Occlusion Myocardial Infarction).

A picture is worth 1,000 words. I illustrate the ECG finding of T-QRS-D below in Figure-3, which I've excerpted from My Comment in the November 14, 2019 post in Dr. Smith's ECG Blog. I’ve taken the lead V3 examples in Figure-3 from previous cases posted on Dr. Smith’s ECG Blog:
  • TOP in Figure-3 — Despite the marked ST elevation in this lead V3 — this is not T-QRS-D, because there is well-defined J-point notching (BLUE arrow). This patient had a repolarization variant as the reason for ST elevation.
  •  BOTTOM in Figure-3 — This is T-QRS-D, because in this V3 lead there is no J-point notching — and, there is no S wave (RED arrow showing that the last QRS deflection never descends below the baseline to form an S wave).

Figure-3: Comparison between ST elevation in lead V3 due to a repolarization variant (TOP — from 4/27/2019) — vs acute OMI (BOTTOM — from 9/20/2015), which manifests T-QRS-D (See text).


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What is MINOCA? 
I suspect the entity known as MINOCA (MI with Non-Obstructive Coronary Arteries) — is not fully appreciated by many clinicians.

  • I was surprised to learn that an estimated 5-15% of patients (depending on the studied population) who are diagnosed with either STEMI or NSTEMI — turn out to have MINOCA, in which cardiac catheterization fails to reveal any infarct-related artery (ie, no "culprit" vessel with at least 50% stenosis) — and no clear systemic etiology is found to explain the patient's presentation to the hospital (Tamis-Holland et al: AHA Scientific Statement on MINOCA — Circulation 139:e891-e908, 2019 — Broncano et al — RadioGraphics 41:8-31, 2021 — and — Sykes et al — Interventional Card Review 16:e10, 2021).

I was therefore intrigued by today's case — in which an older woman presented with syncope and cardiac arrest (but no chest pain) — with the ECG shown in Figure-2 (as well as anterior wall akinesis on Echo) — but without any obstructive coronary disease on cardiac catheterization.
  • Because all emergency providers will periodically encounter MINOCA (ie, the 5-15% estimated incidence of MINOCA that I cite above in patients initially diagnosed as having a STEMI or NSTEMI) — I've added Figure-4, which summarizes the more common entities associated with MINOCA (This Figure previously published in My Comment in the November 30, 2022 post in Dr. Smith's ECG Blog).
  • An all-too-common misconception is that the absence of obstructive coronary disease on cardiac catheterization rules out acute coronary occlusion as the cause of the patient's acute event. This is not the case. Non-obstructive coronary disease at the time cardiac cath is done does not necessarily imply there was no plaque rupture with thrombus. This is because non-obstructive plaques can fissure, thrombose, totally (or near totally) occlude, have autolysis (spontaneous lysis of thrombus with reperfusion) — yet have less than 50% obstruction at angiography. 
  • Such plaques will often not be recognized as "culprits" — because no fissuring or ulceration is seen. As a result — determination of plaque disruption in such patients can only be diagnosed by use of intracoronary imaging — with either higher-resolution OCT (Optical Coherence Tomography) or IVUS (IntraVascular UltraSound).

  • KEY Clinical Point: Despite lack of obstructive coronary disease on cardiac catheterization — the most common cause of MINOCA is still probably an acute OMI that has spontaneously reperfused (but which is simply no longer evident by the time cardiac cath is performed).

Additional Points about MINOCA:
I found it surprising to learn that the initial description of acute MI despite normal coronary vessels is not a new concept — having been first described ~80 years ago (with eventual adoption of the term, "MINOCA" in 2013).
  • The 3 most common Causes of ACS (Acute Coronary Syndrome) without coronary disease are: i) Myocarditis (up to 1/3 of these patients); ii) Takotsubo cardiomyopathy; and, iii) MINOCA.
  • There is a trend toward these patients being younger — with a greater relative percentage of women — and fewer traditional cardiac risk factors.
  • Longterm prognosis of patients with MINOCA clearly depends on the underlying etiology. That said — it's important to appreciate that this entity is not benign, with similar mortality as for patients with obstructive coronary disease following their infarction.

  • Cardiac MRI — provides an answer to the etiology of patients with MINOCA in more than 2/3 of cases. 
  • Cardiac MRI successfully identifies ~80% of patients with acute myocarditis by picking up evidence of inflammation — with the distinct advantage of being noninvasive compared to endomyocardial biopsy.
  • Use of LGE (Late Gadolinium Enhancement) — is routinely recommended with cardiac MRI to increase diagnostic yield, as a means to identify fibrosis and other abnormalities in cardiac tissues.
  • Cardiac MRI (especially with the addition of LGE) provides insight to longterm prognosis of patients with MINOCA.

Figure-4: Classification of Underlying Diagnoses in Patients with MINOCA (Adapted from Table-1 in Sykes et al: Interventional Cardiology Review: 16:e10, 2021). 

NOTE: As per Sykes et al — The entities listed under "Other Etiology" may be diagnosed following further investigation and should be considered separately (because they are typically associated with myocardial injury but not considered an MI by the 4th universal definition of MI). This is an important indication for cardiac MRI in patients suspected of MINOCA. 

KEY Clinical Point: 
Despite lack of obstructive coronary disease on cardiac catheterization — the most common cause of MINOCA is still probably an acute OMI that has spontaneously reperfused (but which is simply no longer evident by the time cardiac cath is performed).



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Acknowledgment: My appreciation to Arlind Dragoshi (from Tirana, Albania) 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 #183 — Reviews the concept of deWinter T-Waves (with reproduction of the illustrative Figure from the original deWinter NEJM manuscript).

  • ECG Blog #218 — Reviews HOW to define a T wave as being Hyperacute? 

  • ECG Blog #193 — 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 Blog #194 — Reviews how to tell IF the “culprit” (ie, acutely occluded) artery has reperfused using clinical and ECG data.

  • ECG Blog #228 — Reviews the concept of "Silent" MI.

  • ECG Blog #215 and ECG Blog #318 — Review of cases with T-QRS-D.

  • The November 14, 2019 post in Dr. Smith’s ECG Blog (Please scroll down to the BOTTOM of the page for My Comment and illustration of the phenomenon of T-QRS-D = Terminal QRS Distortion).
  • The November 15, 2023 post in Dr. Smith’s ECG Blog (See My Comment at the bottom of the page regarding MINOCA).