An elderly woman with acute chest pain -- real or fake ST Elevation?

Written by Pendell Meyers

An elderly female called EMS with acute chest pain. 

Her vitals were within normal limits, and here is her EMS ECG:

What do you think?

Sinus rhythm, and QRS shows likely subtle RBBB, plus LAFB. While some STE could be expected by the large wide S wave in inferior leads, there is is STE and possibly HATW in II, III, and AVF, with reciprocal findings in aVL. While STD could be expected after a large R' of a RBBB in V2, that is not the case here: there is no R' in V2. So the STD in V2 is not explained, and is very large in proportion to its QRS complex, concerning for posterior OMI. The T waves in V4-6 are also a bit suspicious for hyperacute T waves. Overall, I would have high confidence for at least inferior and posterior OMI.

Queen of Hearts interpretation:

OMI with high confidence

Explainability image: 

I agree that the posterior OMI findings in V2 are the single most specific lead in this case.

It sounds like her pain improved before her first ECG obtained in the ED:

In context of the first ECG and resolution of symptoms, this shows reperfusion. however, if I interpreted this ECG alone and without context, I would have said it is nonspecific. This ECG is showing relative reperfusion compared to the first, and it briefly can pass through normal or near-normal before transitioning to reperfusion pattern.

QOH also sees no clear signs of active or reperfused OMI on this ECG (she cannot incorporate context or prior ECGs, yet).


Initial troponin (high sensitivity trop I): 212 ng/L.


She underwent angiogram within a few hours and was found to have mid-RCA culprit lesion, 99% stenosis, TIMI 3 flow. PCI was performed.

Here is her ECG several hours later:

Inferoposterior reperfusion findings.

Her peak troponin (high sensitivity trop I) was 23,893 ng/L.

Smith: 

This result shows you that troponin tells you what happened hours ago, not what is happening right now!  The artery was open, but the troponin rose from 212 to 23,000.  This patient was lucky to have spontaneous reperfusion.  Activating the cath lab so that the patient goes to angiogram "within a few hours" is too slow unless there is reperfusion.  I don't know if the delay was because they did not diagnose the OMI on the first ECG, or because they recognized reperfusion (by the ECG or pain resolution or both) on the second one.  If the latter, than the management was good.  If the former, then they could have risked an even larger MI than occurred.

What tells you the state of the artery right now?

1) The ECG with active ischemia or reperfusion or subendocardial ischemia or nonspecific (no ischemia)

2) presence or absence of symptoms.

(A specific finding on the ECG is much more reliable than symptoms)

What does not tell you what is going on right now? Rather, they tell you what has been going on in the last several hours:

1) Echocardiogram -- The myocardium remains stunned and hypokinetic after reperfusion.

2) Rising troponin -- troponin leaks from infarcted myocardium for a long time after ischemia is gone and will rise for a long time.

Queen of Hearts Update

We are working on upcoming models that are finally able to give more than a dichotomous yes/no for OMI. The most important distinct choices we will train first, are: 

Active OMI

Reperfused OMI

Subendocardial ischemia

Our very first such model correctly marks the first ECG in this series as "Active OMI, high confidence", and the last ECG as "Reperfused OMI, high confidence."

More to come!

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MY Comment, by KEN GRAUER, MD (12/10/2024):

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There are 2 aspects of today’s case that I found especially interesting: i) How despite the unusual appearance of the initial ECG — we knew there was acute OMI (TOP tracing in Figure-1); — and, ii) Some unexpected findings in ECG #2 (MIDDLE tracing in Figure-1).

Today’s Initial ECG:

As per Dr. Meyers — ECG #1 is diagnostic of acute OMI. The rhythm is sinus — and there is bifascicular block (RBBB/LAHB). That said — there are some atypical features:

In this older woman with new CP (Chest Pain) — my "eye" was immediately drawn to the 2 leads within the RED rectangles. 

• Regarding the inferior leads — there clearly is ST elevation in leads III and aVF, albeit with a saddleback shape that is often benign. In contrast — the T wave in lead II looks hyperacute (larger in size, with a disproportionately wide base — in comparison to modest dimension of the QRS in this lead).
• But any doubt that I may have had from the saddleback shape of ST elevation in leads III and aVF — was immediately dispelled by the shape of ST-T wave depression in lead aVL, which manifests a precise mirror-image opposite picture of the ST-T wave in lead III. In this older woman with new CP — there is no way lead aVL does not indicate acute OMI until proven otherwise.

As always — support in favor of acute inferior OMI can be forthcoming if there is also indication of acute posterior OMI.

• In ECG #1 — There is no way the distinct "shelf-like" flattened ST depression with terminal T wave positivity that we see in lead V2 is not indicative of associated posterior OMI until proven otherwise (within the 2nd RED rectangle).
• Instead of the gently upsloping, slight ST elevation that we normally see in lead V3 — the isoelectric flattened ST segment that we see in neighboring lead V3 confirms posterior OMI (BLUE arrow in this lead).

But what about the QRS widening in ECG #1?

• It is only if you look closely that we realize QRS width is ≥0.14 second (!) in ECG #1 (with true QRS width perhaps best appreciated by measuring QRS duration of the 1st complex within the RED rectangle in aVL).
• While RBBB/LAHB is clearly the best designation for QRS morphology in ECG #1 — the r' deflection is tiny and limited to lead V1 — and the rS complexes in leads V1-thru-V4 look surprisingly narrow. It could be easy to overlook the RBBB in this initial tracing.
• 
  
• P.S. — Could there be RV involvement? Whereas normally there is some ST-T wave depression in lead V1 with RBBB — there is none in ECG #1. In the setting of acute infero-postero OMI — this raises the question of whether there may be associated RV involvement? (which could be clinically relevant, depending on this patient's hemodynamic status).
• Obtaining right-sided leads would have been insightful ...

Figure-1: Comparison between the 3 tracings in today’s case.

What about ECG #2?

The "good news" in today's case — is that the patient's CP had decreased at the time ECG #2 was recorded, in association with near-return to the baseline for the inferior lead ST elevation — and, for the ST depression that had been seen in lead aVL. But what about the chest leads?

• I was puzzled by the appearance of new Q waves in leads V2,V3 (within the dotted BLUE ovals in these leads) — as well as by what appeared to be the suggestion of some new ST elevation in lead V1 that was not seen in ECG #1 (BLUE arrow in lead V1 of ECG #2).
• The increased size of the T waves in leads V2,V3 might be consistent with the limb lead changes suggesting some spontaneous reperfusion — But why the anterior Q waves and new ST elevation in lead V1?
• I suspected this patient might have multi-vessel disease and a changing pattern of collateral flow — but was content for the moment with the "good news" of clinical improvement and plan for prompt cath with PCI.

Putting It All Together

As per Dr. Meyers — the case ended well with cardiac cath showing an RCA "culprit" which was successfully stented. ECG #3 was obtained several hours after PCI.

• Both the anterior Q waves and the suggestion of ST elevation in lead V1 that we saw in ECG #2 are no longer seen in ECG #3.
• Wouldn't today's story "fit" better with events — if we didn't have to explain the above findings in ECG #2?

So — If we only had ECGs #1 and #3 for today's case:

• ECG #1 in this older woman with new CP — is immediately diagnostic of acute infero-postero OMI (in association with RBBB/LAHB).
• ECG #3 — is consistent with successful PCI when compared directly to ECG #1, in that it shows reperfusion ST-T wave changes (resolution of inferior lead ST elevation, now with T wave inversion in III and aVF — and taller, reperfusion T waves in leads V2,V3).
• P.S. — I'm curious if cardiac cath showed multi-vessel disease.

Are there hyperacute T-waves? And how can we know?

A 50-something man presented with worsening severe exertional chest pain which was just resolving as he had an ECG recorded in triage.

Time zero.

Are the T-waves in leads I and II hyperacute?  

Hard to tell. 

How can we know?

By the evolution of the ECG! 

Watch what happens as the heart recovers from its episode of ischemia. The T-waves deflate, demonstrating that the first one was indeed hyperacute.

2 hours

T-waves in lead II are significant smaller

In lead I not much difference

Troponins returned elevated, so the patient was scheduled for urgent angiography.

3 hours

Now they are smaller in both leads I and II.

But also in lead aVL

Post Angiogram

Next day

T-waves are smaller in many leads now, including V4-6.

Lead II, all in sequence

Troponins over 26 hours, from right to left:

Echocardiogram:

Mild concentric left ventricular wall thickening, normal cavity size, and

normal systolic function.

The estimated left ventricular ejection fraction is 64%.

There is no left ventricular wall motion abnormality identified.

Angiogram:

Severe two-vessel coronary artery disease of a left dominant system including 70 to 80% stenosis involving the distal left main/bifurcation.  This is the culprit for the patient's non-ST elevation myocardial infarction

AV groove circumflex, proximal LPDA, and mid LAD stenoses may also be

hemodynamically significant

Occlusion of the proximal nondominant RCA is not likely clinically relevant.  

Smith: not sure why that is.  The ECG shows inferior ischemia.

Heart Team evaluation with preference for urgent coronary artery bypass grafting in the setting of elevated syntax score (30), young patient age, and stenosis involving the left main bifurcation and a left dominant system

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MY Comment, by KEN GRAUER, MD (12/6/2024):

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To paraphrase a famous saying: The ischemic process "is often just a matter of time". Today's discussion by Dr. Smith is highly insightful in showing how dramatically the timing of the ECG (or hopefully ECGs) that we obtain may be with respect to the ECG picture that we receive.

Today's patient is a 50-something year old man who presented with increasingly severe exertional angina, for which his CP (Chest Pain) was just resolving at the time his initial (triage) ECG was recorded (TOP tracing in Figure-1).

• BUT — How often do patients present for evaluation in this timely a manner?
•   How many of the patients that YOU see wait 2 hours? — or 3 hours? — or longer?
•     How many patients do not present to the ED until the next day?

QUESTION:

• What is the usual treatment that all-too-many of these patients receive, if they are among those who delay their visit to the ED for 2 or 3 hours (or longer)?
• 
  
• KEY Point: Dr. Smith skillfully illustrates how the ECG picture we see is so often "a matter of timing" — depending greatly on when each ECG is obtained with respect to the relative degree of CP the patient is experiencing at the time each particular ECG is recorded.
• Implicit in Dr. Smith's discussion, is how important it is to compare serial ECGs in the context of this relative CP severity.

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ANSWER: If the timing is "wrong" (ie, If enough time has passed after CP resolution) — then the ECG may look fairly normal, and the patient's ischemic episode may be overlooked (ie, "pseudonormalization" ).

I limit my comments to comparison of just 2 of the 5 ECGs in today's case. I've labeled KEY findings in the initial ECG (TOP tracing in Figure-1). No labeling of the bottom ECG is needed for comparison between the 2 tracings. 

• Given the history of resolving CP in a patient with recently increasing anginal severity — My "eye" was immediately drawn to the T wave in lead II of ECG #1 that simply stated, looked "too big" for its QRS (within the RED rectangle in lead II).
• In the context of this hyperacute T wave in lead II — the T waves in lead I and lead aVL also looked disproportionate to the QRS complex in these respective leads (the T wave in lead I being more than half the height of the QRS in this lead — and the T wave peak in lead aVL being "fatter"-than-expected, with a T wave base that is wider-than-expected, considering the R wave in this lead).
• My "eye" was next drawn to the deep, symmetric T wave inversion in lead V1, that is perhaps as deep of an isolated T wave inversion in lead V1 that I have seen (within the RED rectangle in V1).

In the context of a recent anginal CP episode — I knew that the T waves in leads II and V1 clearly represent an acute process until proven otherwise. The appearance of all other leads in this initial ECG need to be interpreted with the knowledge that ECG #1 is definitely abnormal!

• In marked contrast to the exceedingly deep T wave inversion in lead V1 — is the subtle-but-real J-point depression in leads V2 and V3. Considering that these 2 leads normally manifest slight gently upsloping ST elevation — this J-point depression (especially with the T wave flattening in lead V2) suggest posterior involvement until proven otherwise (these slightly depressed J points highlighted between opposing BLUE arrows in these leads).
• Whereas in isolation, it might be difficult to distinguish between a repolarization variant vs hyperacute T waves in the 4 leads with blue question marks — in the context of knowing that all the leads so far mentioned are clearly abnormal — I interpreted the T waves in leads aVF; V4,V5,V6 as also hyperacute.

Which leads me to the ST-T wave appearance in leads III and aVR (the PURPLE question marks). 

• Normally, with DSI (Diffuse Subendocardial Ischemia) — there is ST depression in multiple leads with ST elevation in leads aVR>V1 (with occasional ST elevation also in lead III). But in today's initial ECG — we essentially see the opposite ECG picture in this patient who had been having a severe anginal episode that has just now resolved at the time ECG #1 is recorded!
• I interpreted these ECG findings as, if not indicative of a recent event — then consistent with DSI in a patient with multivessel disease (albeit difficult to localize a "culprit" given how generalized these ST-T wave findings are).

Dr. Smith's discussion above follows serial ECG evolution over the course of 5 tracings.

• That said — I thought straight comparison between the 1st and last ECGs in this serial evolution (as I show in Figure-1) — to be humbling in making us better appreciate the matter of "timing" in our assessment of patients whose CP may have decreased by the time we get to see them.
• We need to remember to include notation of the presence and relative severity of CP at the time that each ECG in a CP patient is recorded.

P.S.: Did YOU notice the S1Q3T3 pattern in the 2 ECGs shown in Figure-1?

• Although the T wave in ECG #1 is only shallowly inverted — this still qualifies as an S1Q3T3. The S1Q3T3 is more distinct in ECG #5.
• PEARL: Keep in mind that an S1Q3T3 pattern in the absence of a suggestive history and other ECG findings of acute PE is a purely nonspecific sign. By itself — seeing this ECG pattern does not necessarily mean that the patient has a pulmonary embolism. 

Figure-1: I've reproduced and labeled today's initial ECG — with comparison to the repeat ECG done the next day.

What can you find with continuous ST monitoring in the ED?

This was written by one of our fine residents, who will soon be an EMS fellow: Michael Perlmutter

Case

A mid-50s male came to the ED with a burning sensation that was acutely worse while at home. He had recently returned from overseas travel where these symptoms had been intermittently bothersome over the preceding weeks and had been attributed to heartburn.

The previous evening, he was at rest and developed severe pain with associated shortness of breath, diaphoresis and a brief syncopal episode. He had ongoing pain following the syncopal event but went to bed and awoke in the morning with ongoing pain.

He came to the ED at the urging of his wife. At ED presentation, he was asymptomatic but developed extremely brief periods of recurrent burning discomfort that were centered about the sternal notch.

Given his history, an EKG, labs including high sensitivity troponin, and chest radiograph were ordered. 

Here is the first ECG at Time zero:

Here is his initial EKG: What do you think?

Smith: this was shown to me without any other information, and I said that it is strongly suggestive of inferior OMI, probably reperfused. There is minimal STE in lead III with reciprocal STD in aVL. The terminal part of the T-wave is inverted in lead III, and reciprocally terminally upright in lead aVL.

I put this through the Queen of Hearts and was shocked that she did not see it.

Case continued

A bedside cardiac ultrasound revealed grossly preserved left ventricular function, no appreciable wall motion abnormality, pericardial effusion, or obvious valvular abnormality. His initial high sensitivity troponin I returned at 1300 ng/L and given that his cardiac workup was otherwise unremarkable, a CT was obtained to evaluate for pulmonary embolism and aortic aneurysm or dissection but this too was unrevealing. Another EKG was also obtained.

ECG at time 82 minutes:

What do you think? 

Smith: all STE in lead III is gone, as is the STD in aVL. This dynamic change is diagnostic of ACS. And so, of course, is the elevated troponin.

Cardiology was consulted and agreed that his history was high risk for ACS and a next-day angiogram was merited. He was started on intravenous heparin and given aspirin. His care was signed out to the overnight team with a plan to continue to obtain serial troponin measurements and admit the patient to the hospital for an angiogram. 

Overnight, his troponin continued to rise, but he remained asymptomatic and was resting between cares. When pressed, he endorsed mild, very brief periods of a retrosternal burning sensation and serial ECGs were obtained.

time zero: 1378

1 hours: 1436

4 hours: 1651

6 hours: 1750

8 hours: 1850 

Smith: But rising troponins only tell you about the past, not about the present moment!!

ECG at 8.3 hours

Now completely normalized

What is noticeable now? 

The first EKG was concerning for a Wellen’s-like pattern of subtle reperfusion changes in the setting of stuttering anginal-equivalent symptoms, but none were diagnostic of STEMI or OMI.

Later in the night, the patient became bradycardic and developed a Mobitz II pattern, but he remained asymptomatic and hemodynamically stable. Very early in the morning, he reported recurrence of a heartburn sensation, so another EKG was obtained. 

ECG at 9 hours:

What do you think?

Smith: the STE with reciprocal STD in aVL is back.  In addition, there are now hyperacute T-waves in the inferior leads.  There is also a bit of new ST Elevation in right precordial leads: is there also some Right ventricular involvement?

This was also non-diagnostic for OMI, although the dynamic changes are diagnostic of ACS. However, with the development of Mobitz II and ongoing stuttering symptoms, the 12-lead EKG was left attached to the patient and was observed.

After about 10-15 minutes, there was a significant change and very large inferior ST elevation with reciprocal ST depression in the lateral leads was observed and the patient was moved to the stabilization room. 

ECG at 11 hours:

No comment needed

Given this EKG with diagnostic findings, his heparin infusion was stopped, and he was given a 5000 unit heparin bolus and 180 mg of ticagrelor while the cardiac catheterization laboratory was activated and interventional cardiology was emergently consulted. 

Angiography was performed and found a normal LAD, a large co-dominant LCX, and 95% disease at the mid-RCA. A large RPDA and a small RPAV giving rise to RPL1 was seen. The RCA was stented successfully with TIMI III flow noted post-procedure and the patient has done well with a post-PCI TTE demonstrating good LVEF and no wall motion abnormality. Given the right coronary anatomy seen during angiography, it is particularly interesting that subtle T wave changes were seen on the previous EKGs in the high lateral leads that would otherwise only be expected with a more proximal RCA lesion. 

This case highlights the importance of maintaining a high degree of suspicion for clinically important disease even in the absence of classic symptoms or an EKG without STEMI despite an initially high troponin.

This case highlights the value of continuous 12-lead EKG monitoring, which is not routinely available in many institutions but proved invaluable in making a timely diagnosis at the time that the EKG became diagnostic. 

Smith: There is a misconception that uptrending troponin had an effect on the decision to go to the cath lab. It really should have little influence on us. A rising troponin just tells us what was happening hours ago. A good size infarct that no longer has active ischemia will have continually rising troponins due to the damage that was done hours ago. The only way to know if this patient whom you know has Acute MI needs the cath lab is if 1) symptoms are present and can't be controlled or 2) the ECG shows active ischemia. Also: electrical instability, pulmonary edema, or hypotension.

In this case, there was electrical instability (Mobitz II block). That alone is enough to activate the cath lab.

This apparently did not prompt cath lab activation, but it did lead to continuous ECG monitoring which led to the ECG which mandated cath lab activation.

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MY Comment, by KEN GRAUER, MD (12/3/2024):

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Today’s case is a study in important subtlety — from which much can be learned in retrospect.

• The 1st question that arises — Is whether or not either of the first 2 ECGs might be diagnostic of an acute inferior OMI?
• Perhaps the more clinically important question is — How can we learn retrospectively what might have been done better. While fully acknowledging that, "Hindsight is 100% in the retrospectoscope" (ie, from the comfort of my computer desk chair)  — I think it insightful to relook at the 4 serial tracings shown in this case.
• 
  
• NOTE: Mention is made that a total of 10 serial ECGs were recorded in today's case over an 11-hour span. I only have access to the 4 ECGs that I show in Figure-1 — plus the final ECG done at T = 11 hours, at which time dramatic and diffuse hyperacute ST elevation is seen. I limit my comments to the history provided and the 4 ECGs shown in Figure-1.

Figure-1: I've labeled the first 4 ECGs shown in today’s case.

My Initial Thoughts on Today's CASE:

The history in today's case is of a mid-50s man with CP (Chest Pain) that apparently had been going on intermittently for some period of time (weeks?) — with a more severe episode the night before presentation. The patient noted a "brief syncopal period". His CP returned that morning — but CP was not present at T = 0 when ECG #1 was recorded.

• Given this history (with the intermittent nature of this patient's symptoms) — anything might be seen on the initial ECG. It is therefore important to realize that even IF this patient was having an ongoing cardiac event — We might not necessarily see obviously acute changes. 
• Instead, what might be seen — is a certain amount of "pseudo-normalization" (ie, if some degree of spontaneous reperfusion had at some point occurred). We should therefore be prepared to look for subtle ECG findings that may be important — with need to correlate the presence and severity of symptoms with each of these serial ECGs in order to optimally understand what happened.

The Initial ECG in Figure-1 (done at T = 0):
The rhythm in ECG #1 is sinus at ~65/minute. All intervals (PR, QRS, QTc) and the frontal plane axis are normal. There is no chamber enlargement.

• As will become important momentarily — the PR interval = 0.20 second in ECG #1 — the frontal plane axis = +50 degrees — and the patient had no CP at the time this tracing was recorded.
• In ECG #1 — 3 leads show findings of potential concern: i) The most concerning finding is seen in lead III (within the RED rectangle) — in which there is slight-but-real ST elevation (RED arrow), with a biphasic T wave ending in terminal negativity.
• ii) That this ST-T wave abnormality is "real" — is supported by reciprocal changes in high-lateral leads aVL and I (BLUE arrows highlighting ST segment straightening, with a hint of ST depression in these leads).
• In the chest leads — there is T wave "imbalance", in that the upright T wave in lead V1 is taller than the upright T wave in lead V6. As I emphasize in My Comment in the June 1, 2022 post in Dr. Smith's ECG Blog — such "T wave imbalance" is a nonspecific finding that I have on occasion found useful as a "tip-off" to an acute coronary syndrome that I might not otherwise have recognized.
• 
  
• BOTTOM Line: While I found interpretation of ECG #1 to be non-diagnostic for OMI as a single tracing — given the history, I thought the subtle abnormal findings in leads I,III,aVL and the precordial T wave "imbalance" — could reflect a certain amount of "pseudo-normalization" (from spontaneous reperfusion) in a patient with a recent event, especially since the patient had no CP at the time ECG #1 was recorded!
• Suggestion: Given how quickly ECG findings may change in an acute coronary syndrome of uncertain duration — I favor not waiting more than ~20 minutes for the initial repeat ECG (with additional repeat tracings in short succession until there is clear indication of no progression).

The 2nd ECG in Today's Case (ECG #2 was done at T = 82 minutes):

While unknown if the patient was (or was not) having CP at the time ECG #2 was recorded — the initial Troponin came back significantly elevated at 1300 ng/L.

• My reason for noting the slight shift in frontal plane axis in ECG #2 (ie, from +50 to +70 degrees) — is because there is subtle-but-real change in ECG appearance for the leads mentioned above in ECG #1 — and we want to ensure that a change in frontal plane axis is not responsible for this (I did not think this slight change in axis was the cause for the change in limb lead ST-T wave appearance).
• Specifically: i) Despite no significant difference in QRS morphology — there is no longer any ST elevation in lead III; — and, ii) There is no longer any hint of ST depression in leads I and aVL — and T wave amplitude has increased slightly in both of these leads.
• While fully acknowledging the subtlety in these limb lead ST-T wave changes — the fact that 3 leads show similar evolution to me suggests that these changes are "real" — and may reflect "dynamic" ST-T wave change. Given the elevated Troponin (= 1300 ng/L) — Hasn't the diagnosis of acute OMI (and the need for prompt cath) been made?

The 3rd and 4th ECGs (done at T = 8.3 hours — and T = 9 hours):

The patient apparently continued to have ongoing stuttering symptoms (recurrence of a "heartburn" sensation) during the night. At some point — the patient became bradycardic and developed a "Mobitz II pattern" — but he remained asymptomatic and hemodynamically stable.

In the interest of pointing out subtle but relevant issues in today's case — I'll note the following:

• Despite no more than slight axis adjustments — the limb leads in ECG #3 and ECG #4 continue to show ongoing changes of coronary reperfusion. These include: i) Progressive increase in T wave amplitude in leads III and aVF (compared to ECG #2); — and, ii) Progressive decrease in T wave amplitude in lead aVL (compared to ECG #2).
• 
  
• Note the serial change in the ST-T wave appearance in lead V1 over the course of the 4 ECGs in Figure-1. Although we usually associate development of a Wellens'-like sharp T wave descent into terminal T wave negativity in leads V2,V3,V4 with Wellens' Syndrome — here we see this evolution only in lead V1. In retrospect — I interpreted these serial lead V1 ST-T wave changes as support of the early precordial T wave "imbalance" as a "tip-off" finding that I noted when interpreting ECG #1.
• Note also development of distinct J-point notching in leads V3,V4 that was not seen earlier. As per My Comment in the February 2, 2024 post — knowing the results of today's cardiac catheterization, I retrospectively interpreted this finding as representing ischemic Osborn waves.

The Patient developed AV Block, "Mobitz Type II" during the Night ...

Realizing that no definitive diagnosis of the nature of the conduction block referred to in description of today's case can be made without seeing the actual ECG rhythm strips — I'll suggest that statistical odds that the type of AV block seen was Mobitz I (and not Mobitz II) are well over 90-95%.

• Today's patient was found on cath to have RCA OMI. Mobitz I is common in this clinical setting. Mobitz II is not. This is especially true because: i) The QRS complex is narrow in all 4 ECGs seen in Figure-1 (whereas the QRS is usually wide with Mobitz II); — and, ii) The first 2 ECGs in today's case show a normal PR interval ( = 0.20 second) — whereas ECG #3 and ECG #4 now show 1st-degree AV block (PR interval = 0.24 second). It is common for Mobitz I in the setting of inferior OMI to evolve from a normal PR interval — to 1st-degree AV block — to 2nd-degree, Mobitz I. This sequence of evolution is not seen with Mobitz II — that typically presents with abrupt failed conduction despite a constant (and usually normal) PR interval.
• What most likely was seen during the night — was 2nd-degree AV block with 2:1 AV conduction, which is often mistakenly interpreted as Mobitz II (because the PR interval remains constant as every-other-beat is non-conducted). Technically — one can not distinguish between Mobitz I vs Mobitz II when there is 2:1 AV conduction — because you never see 2 consecutively conducted beats (so you never know whether the PR interval would progressively increase before dropping a beat IF given a chance to do so). That said — in the setting of acute inferior OMI with a narrow QRS and evolution from a normal to a prolonged PR interval — the odds that 2:1 AV block represent Mobitz I are overwhelming. (For more on ECG recognition and clinical significance of 2nd-degree AV blocks — Please check out My Comment at the bottom of the page in the November 12, 2024 post in Dr. Smith's ECG Blog).
• 
  
• Clinical Relevance: On seeing PR interval lengthening during the night — that evolved into 2:1 AV block — We had at that time, yet one more piece of evidence diagnostic of acute inferior OMI in progress.