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).
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• ECG Blog #218 — Reviews HOW to define a T wave as being Hyperacute? 
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• 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.
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• ECG Blog #228 — Reviews the concept of "Silent" MI.
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• ECG Blog #215 and ECG Blog #318 — Review of cases with T-QRS-D.
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• 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).

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.
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• 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).