A woman in her 50s with chest pain and lightheadedness and "anterior subendocardial ischemia"

 Written by Pendell Meyers

A woman in her 50s presented with acute chest pain and lightheadedness since the past several hours. Here is her triage ECG during active symptoms:

What do you think?

The ED physician read this as "Normal sinus rhythm. LVH. Marked ST abnormality, possible anterior subendocardial injury."  

Smith: I suspect this was a confirmation of the conventional computer interpretation.  These are often wrong and lead the physician astray.

This is wrong on many levels. 

The rhythm is some form of heart block (see Ken's comments at end of post) with junctional escape. The STD maximal in V1-V4 is diagnostic of acute transmural posterior wall ischemia, most likely due to posterior OMI. Subendocardial ischemia does not localize, and subendocardial ischemia presents with STD maximal in V5-6, II, and STE in aVR.

Here is the Queen of Hearts AI interpretation:

I'm really surprised the confidence isn't higher, I've seen QOH be more confident on more difficult ones that this. Anyway, she does say OMI.

So the patient's OMI was initially missed. It does not meet STEMI criteria. 

Luckily, 45 minutes later, with ongoing pain and a troponin I that resulted at 136 ng/L, the ECG was repeated:

What do you think now?

Easy for anyone.

Obvious STEMI(+) OMI of inferior, posterior, and lateral walls, now with likely 2nd degree heart block type 1 (Wenckebach).

Finally the OMI was realized.

She was taken to cath and found to have total mid RCA occlusion, TIMI 0 flow, stented with excellent result. 

Her heart block resolved quickly. 

Troponin quickly rise to greater than 25,000 ng/L (the lab's reporting limit). 

Echo showed matching wall motion abnormalities.

She survived to discharge.

Learning Points:

We can find OMI on ECG much sooner than STEMI criteria in many cases, and of course many OMIs never meet STEMI criteria at all.

AI can do it too. 

STD maximal in V1-V4, without a QRS abnormality causing it, and in the setting of ACS symptoms, is posterior OMI until proven otherwise.

Subendocardial ischemia does not localize.

The RCA usually supplies the SA and AV nodes, so RCA OMIs can present with heart blocks and bradycardias like in this case.

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MY Comment, by KEN GRAUER, MD (7/30/2023):

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There are numerous important points that are brought out by today’s case. For our readers who enjoy the challenge of interpreting cardiac arrhythmias — today’s case offers a “gold mine” of PEARLS regarding the recognition of AV Wenckebach. 

• WARNING: What follows below illustrates my “thought process” in evaluating today’s initial rhythm. Some of the concepts I review are basic, and should be understood, learned and applied by all providers who regularly follow Dr. Smith’s ECG Blog. Other concepts I’ll review go well beyond the basics — and are aimed at advanced interpreters (and those who want get better at interpreting complex rhythms).
• I leave for YOU to decide how deeply you want to “dive” into today’s rhythm. That said, even for less experienced interpreters — KNOW that I clarify KEY basic concepts important for all providers to appreciate. 

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NOTE: I initially only saw ECG #1 — knowing only what the ED physician wrote in his interpretation. I knew nothing else about the case (For clarity — I've reproduced today's initial tracing in Figure-1).

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Figure-1: I have reproduced the initial ECG in today’s case.

PEARL #1: Although the rhythm in ECG #1 is complex and extremely challenging — You do not need to figure out what this rhythm is, in order to appropriately manage the patient! 

• So — No worries if you did not recognize AV Wenckebach until later (or even if you never recognized AV Wenckebach at all in today’s case). What counts — is that you appreciate the history ( = ie, A woman in her 50s who presents to the ED with CP and lightheadedness for several hours) — and that you know to immediately elevate your index of suspicion for acute OMI whenever you learn that your patient presents to the ED for new CP! 
• By “elevating” your index of suspicion for acute OMI — I mean appreciating how this history of new CP immediately places your patient in a “higher-prevalence” group for acute OMI — so that you “go on the lookout” for even subtle ECG abnormalities (that in this clinical setting mean acute OMI until proven otherwise).
• In Figure-1 — The ST-T wave abnormality in lead V2 of ECG #1 is obvious. A bit more subtle (but definitely present) — are the ST-T wave abnormalities in neighboring leads (ie, T inversion in lead V1 — ST flattening and depression in leads V3-thru-V5). As per Dr. Meyers — a history of new CP + localized ST-T wave depression that is maximal in leads V2-to-V4 = acute posterior OMI until proven otherwise!
• 
  
• So, to return to Pearl #1 — the reason it does not matter if you even recognize AV Wenckebach at all in this initial ECG — is that assuming this patient is not hypotensive — since the overall heart rate is reasonable and there is ECG evidence that suggests acute posterior OMI until proven otherwise ==> there is indication for prompt cath with PCI as soon as this can be done! The clinical reality — is that any conduction disturbance that might be present, will probably improve (if not resolve) as soon as the “culprit” artery is reperfused!

PEARL #2: Remember that, “Common things are common!” In the setting of acute inferior — or infero-posterior — or isolated posterior OMI — most conduction disturbances that might develop will turn out to be some manifestation of AV Wenckebach (Remembering that “AV Wenckebach” — is a synonym for 2nd-degree AV block, Mobitz Type I ).

• All emergency providers are familiar with the “classic” picture of Mobitz I, 2nd-degree AV block (ie, The PR interval progressively lengthens until a beat is dropped — which produces a slight pause — and then the cycle begins again, as the next beat is conducted with a shorter PR interval).
• That said — there are numerous “variations on this theme” of Mobitz I that when present, can make recognition of Mobitz I quite challenging. Some examples of variation on the "theme" of Mobitz I might include — junctional escape beats, dual AV nodal pathways, simultaneous SA block — or when Wenckebach cycles terminate with PACs or Echo beats, instead of the “classic” non-conducted on-time P wave. NO matter! — because Common things are common. IF your patient has some type of conduction disturbance + an acute inferior or infero-postero or isolated posterior OMI — then even if the “classic” Mobitz I picture is not seen, the chances remain very high that some form of AV Wenckebach is still operative.
• The above statement is especially true IF the QRS complex is narrow (as it is in ECG #1) — since the QRS will almost always be wide when there is Mobitz II.
• Common things are common. In my experience of looking for Wenckebach over the past 40+ years — >95% of 2nd-degree AV blocks are Mobitz I (and not Mobitz II).

PEARL #3: IF you want to try to determine the mechanism of a conduction disturbance — the EASIEST initial step is to label the P waves. You'll note that I also number the beats — since this instantly allows everyone involved to ensure we are all talking about the same part of the tracing (Figure-2).

• For there to be AV block — the atrial rhythm should be regular (or at least almost regular, if there is an underlying sinus arrhythmia). If P wave morphology is changing — or if the P-P interval is clearly irregular — then the chances are that you are dealing with something other than simple AV Wenckebach.
• 
  
• LOOK at Figure-2. Isn’t it much easier now that all P waves are labeled — to appreciate that the underlying atrial rhythm is regular? 
• 
  
• As soon as I labeled all P waves — it became obvious to me that many (most) of these P waves were unrelated to neighboring QRS complexes, which by definition means that there is AV dissociation. 

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

PEARL #4 — AV dissociation is never a “diagnosis”. Instead — it is a condition caused by “something else”. There are 3 Causes of AV Dissociation: i) AV Block itself (of 2nd- or 3rd-degree); ii) "Usurpation" — in which P waves transiently do not conduct because of an accelerated junctional rhythm that takes over (ie, “usurps” control of the rhythm); and, iii) "Default" — in which a junctional escape rhythm takes over by “default” (ie, because of SA node slowing) — as may occur if a medication such as a ß-blocker is being used.

PEARL #5 — Complete AV dissociation is not the same as 3rd-degree AV block! This is one of the most commonly misunderstood concepts in all of arrhythmia interpretation! Complete AV block is just one of 3 possible causes of AV dissociation.

• The KEY to determining if any AV block at all is present — is to determine IF P waves fail to conduct despite having adequate opportunity to do so.

Consider Figure-3. 

• The P waves labeled C, E, G, I, K and M do not realistically have a chance to conduct — because they either occur with a PR interval that is too short (too close to its neighboring QRS) — or the P wave occurs within the QRS — or the P wave occurs too soon after the QRS (within the absolute refractory period — as for M).
• In contrast — the P waves labeled B, D, F, H, J, L, N and P should seemingly conduct — but fail to do so. Therefore, there is at least some form of 2nd-degree AV block in Figure-3.

Figure-3: For clarity — I've denoted P waves by capital letters.

PEARL #6 — The rhythm in Figure-3 is not complete AV block! Most of the time, IF the degree of AV block is complete (3rd-degree) — then the ventricular rhythm should be regular (or at least fairly regular). This is because escape rhythms arising from the AV node, the His or ventricles are usually fairly regular rhythms. Exceptions may occur (ie, during cardiopulmonary resuscitation) — but even then, there will usually be a recognizable pattern of ventricular regularity. 

• Within seconds — I knew that the initial ECG in today's case was not complete AV block.
• 
  
• KEY Point: The BEST clue that there is at least some conduction — is IF in the presence of AV dissociation, you see one or more beats that occur earlier-than-expected.

Take another LOOK at today's initial ECG (which I reproduce in Figure-4). 

• HOW did I immediately know that the rhythm was not complete AV block?

Figure-4: I've reproduced the initial ECG that was shown in Figure-1.

ANSWER:

• I knew the rhythm in Figure-4 was unlikely to represent complete AV block — because beat #7 occurs earlier-than-expected (As shown in Figure-5 — the R-R interval preceding beat #7 = 1040 msec. — whereas the R-R interval preceding all other beats on this tracing = 1160 msec.). As per PEARL #6 — this strongly suggests that beat #7 is conducted.
• Since at least 1 beat is being conducted in Figure-5 — this means that the rhythm is not complete AV block — but instead, some form of 2nd-degree AV block — and by PEARL #2, we know that by far, when there is acute posterior OMI and some form of 2nd-degree AV block with a narrow QRS — that this is almost certain to be some form of AV Wenckebach.
• 
  
• PEARL #7: Not only is the rhythm in this initial ECG not complete AV block — it is also not necessarily a "high-grade" form of 2nd-degree. I define a "high-grade" 2nd-degree block — as when 2-or-more P waves that should conduct, fail to conduct. As discussed above in explanation to Figure-3 — the P waves labeled C, E, G, I, K and M do not realistically have a chance to conduct — because they either occur with a PR interval that is too short (too close to its neighboring QRS) — or the P wave occurs within the QRS — or the P wave occurs too soon after the QRS (within the absolute refractory period — as for M). Therefore — we never see 2 consecutive P waves that should conduct, fail to do so — which means that we have no evidence to suggest this is a high-grade block.

Figure-5: I've measured the R-R intervals in Figure-4.
(8/7/2023 — My THANKS to H.S.Cho for catching my typo ...)

PEARL #8: Realize that IF you want to get good at recognizing complex arrhythmias (especially complex forms of AV dissociation and AV block) — then You HAVE to use calipers. 

• I am not saying that all providers have to use calipers — because as I already emphasized in PEARL #1 — today’s patient has acute posterior OMI until proven otherwise — which means that prompt cath is needed — with the clinical reality that any conduction abnormality that might be present will probably improve as soon as the “culprit” artery is reperfused.
• 
  
• Did YOU realize that beat #7 in Figure-5 occurs slightly early? The chances are that unless you used calipers — that you would not have realized this.
• 
  
• To EMPHASIZE: Using calipers does not slow down your interpretation. On the contrary, using calipers speeds up your interpretation — because you can instantly determine that beat #7 is occurring slightly earlier-than-expected. 
• 
  
• Using calipers also allowed me to quickly determine that the atrial rhythm that I marked out with RED arrows in Figure-2 — is regular! Knowing where to look for those P waves that are partially hidden within QRS complexes or parts of the ST-T wave — is made much easier by setting your calipers to a P-P interval determined by the distance between any 2 consecutive P waves you can clearly identify (such as the distance between B and C — or between C and D in Figure-3). 

PEARL #9: When uncertain if a given beat is or is not being conducted to the ventricles — LOOK for subtle differences in QRS morphology!

• Although both sinus-conducted beats and junctional escape beats are supraventricular impulses that look similar — there sometimes are subtle-but-real differences in QRS morphology between these 2 types of beats! This is because junctional escape beats do not always arise from the center of the AV node — and when they arise either to the right or the left of center, they may manifest subtle differences in morphology (ie, The R wave may be slightly smaller or taller; the S wave may be slightly deeper or wider).
• We see this phenomenon best in lead V5 of Figure-5! BLUE arrows in this lead show that the only beats in the entire rhythm strip with these deeper S waves are beats #7 and #8. This strongly supports my suspicion that beat #7 is sinus-conducted, here with a long 1st-degree AV block (of ~0.42 second).
• 
  
• Acknowlegement I am not sure of the mechanism of beat #8 — because the PR interval that precedes it is slightly shorter than the PR interval of beat #7, which we know is conducted. The BLUE arrow in Figure-5 suggests that beat #8 is also sinus-conducted, perhaps with slight shortening of the PR interval because of the manner in which it ends a 2:1 Wenckebach cycle? Yet beat #8 is preceded by the same R-R interval of 1016 msec. as the other junctional beats. I'm just not certain. 

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LADDERGRAMS:

I'll conclude my comments with my proposed laddergrams in Figure-6 and Figure-7 — for the 2 tracings shown in today's case.

Figure-6: My proposed laddergram for ECG #1. As suggested by my above discussion — the first 6 beats in ECG #1 appear to be junctional escape, at a rate just over 50/minute. As measured in Figure-5 — the slightly shorter R-R interval preceding beat #7 strongly suggests that this beat is conducted (albeit with a long PR interval). The fact that at least 1 beat is conducted in ECG #1 tells us that this is not complete AV block — but instead, must represent some form of 2nd-degree AV block. Given the clinical setting (ie, apparent acute posterior OMI) and the narrow QRS complex — the conduction disturbance is almost certain to represent some form of AV Wenckebach with junctional escape beats. 

(NOTE: The ? at the end of the laddergram in Figure-6 is to acknowledge that although I suspect beat #8 is also sinus-conducted — I'm uncertain why the PR interval is shorter than the PR before beat #7). 

Figure-7: My proposed laddergram for ECG #2. As per Dr. Meyers — ECG #2 makes the diagnosis of acute infero-postero-lateral OMI obvious — because there is now ST elevation in the inferior leads and in lead V6 — with reciprocal ST depression in lead aVL — and a positive Mirror Test, with marked ST-T wave depression in leads V1-thru-V4 (maximal in leads V2,V3).

As shown in the laddergram — the diagnosis of 2nd-degree AV block, Mobitz Type I (AV Wenckebach) — is now much more evident than it was in ECG #1. Virtually all of the "Footprints of Wenckebach" are now present — including: i) Group Beating (ie, 3:2 AV conduction — with repetitive 2-beat groups); ii) Regular atrial rhythm (RED arrows); iii) Progressive increase in the PR interval within each group until a beat is dropped; and, iv) The pause containing the dropped beat is less than twice the shortest R-R interval.

PEARL #10: The fact that indisputable evidence of AV Wenckebach is seen in ECG #2, that was obtained just 45 minutes after ECG #1 — strongly supports my earlier conclusion that ECG #1 did in fact represent some form of AV Wenckebach, in which the presence of junctional escape beats made this difficult to recognize.

Final Point: The reason every-other QRS complex in Figure-7 looks slightly different from the QRS of the 1st conducted beat in each group — is simply a manifestation of some aberrant conduction. Conditions predisposing to aberrant conduction of beats #3,5,7,9 are set up by the pause preceding beats #2,4,6,8 (Ashman phenomenon).

Profound ST depression in II, III, aVF

This 29 year old African American patient was found down, unconscious, not breathing and was given 2 mg of intranasal naloxone by a bystander.  He then received bag-valve-mask ventilations for several minutes until he became responsive.

He had a prehospital ECG that was worrisome to the medics, so they called me to see him at the door.

On arrival to the ED, the patient was diaphoretic, tachycardic. and had dilated pupils. He was alert and oriented.  He remained somewhat altered, and history was not reliable.

His prehospital ECG showed "inferior" ST depression and high voltage, with tachycardia. I did not think it was due to ACS, but we ordered an ED ECG immediately:

What do you think?

There is profound "inferior" ST Depression. Usually, this is reciprocal to high lateral ST elevation which may be very subtle.  But in this case the clinical scenario is not right for acute ACS with OMI, and there is very high voltage, and the patient is very young, (though beware of young patients, even 29 year olds!!, both here and here).  

The precordial findings are typical for a young AA male  See 20 similar cases here.

I suspected no OMI, that this could be due to LVH plus tachycardia.  I was not worried for a coronary etiology.

But I wasn't certain, and so we planned on a Bedside echo (which was normal), and serial troponins.

Looking through the records, we found an ECG from 2 years prior:

There is some similarity in the inferior leads, so I suspected that today's ECG was an exaggeration of this STD

ECG 2 years prior at slower heart rate

At a slower heart rate, there is less STD

I sent today's ECG to the Queen of Hearts (PMcardio OMI), and here is the verdict:

First hs-troponin I returns at 250 ng/L.

4.5 hours ECG:

Not much change

hs troponin I peaks at 500 ng/L

8 hours

Next morning

Urine drug screen: 

Amphetamine, Methamphetamine, Fentanyl, Fentanyl metabolite

Formal Bubble Contrast Echocardiogram:

Indications for Study: Silent Ischemia.

 

SUMMARY

 

Normal left ventricular cavity size.

Normal estimated left ventricular ejection fraction .

No wall motion abnormality .

The estimated left ventricular ejection fraction is 67 %.

The estimated pulmonary artery systolic pressure is 29 mmHg + RA pressure.

Conclusion:

Type II MI probable due to hypoxia and tachycardia from resp arrest and amphetamine use.  Whether the ST Depression on the ECG represents ischemia or not is uncertain, but it does not represent acute coronary syndrome.

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MY Comment, by KEN GRAUER, MD (7/27/2023):

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The most interesting aspects of today’s case are: i) The tale told by the 6 ECGs; and, ii) The surprise finding of positive troponins! 

The Sum is More than Each of its Parts:

If we look back at the initial ECG in today’s case — it’s easy to let one’s attention be “captured” by the inferior lead ST depression (especially the “eye-catching” sharp and deep descent of the ST segment in lead III) + the mirror-image opposite shape of the ST elevation (with overly straight ST segment take-off) in lead aVL. Under most circumstances — this combination of ECG findings would point to an acute event. But — the sum of this initial ECG is more than each of its parts. Regarding specifics of this initial ECG:

• QRS amplitude in multiple leads is huge! Even though I did not know the patient’s age at the time I saw this initial tracing — it was obvious that voltage for LVH would be easily satisfied. The lateral chest lead ST depression (with terminal T wave inversion in leads V4,V5) supports my impression of marked LVH by the typical ST-T wave appearance of LV “strain”.
• 
  
• PEARL #1: The frontal plane axis in this initial ECG is vertical (small amplitude, nearly isoelectric QRS in lead I — in the face of huge inferior lead R waves). Increased voltage and ST-T wave changes of LV “strain” are commonly seen not only in lateral leads, but also in inferior leads in the presence of marked LVH when there is an inferior frontal plane axis. Given my initial “sum” impression of this tracing (ie, marked LVH with LV “strain”) — I did not think the inferior lead ST depression was disproportionate in view of the relatively fast heart rate (of ~90/minute) and the huge inferior lead R waves of >25mm!
• 
  
• Additional notable findings on this 1st ECG included: i) Very deep infero-lateral Q waves (ie, >8mm in lead III!); — ii) A surprisingly tall R wave (>10 mm) as early as lead V2; — iii) ST elevation with an alarmingly straight ST segment takeoff in lead V2; — and, iv) An unusual biphasic T wave appearance in lead V3.
• 
  
• My Impression of this 1st ECG: Taking all of the above findings into account, I thought — The sum is more than each of its parts! Even without yet knowing the full history — I interpreted this 1st ECG as showing marked LVH with LV “strain” — perhaps in an African-American young adult male with a component of a repolarization variant — but not suggestive of acute OMI. I was not expecting troponins to be positive.

The Sum Total of All 6 ECGs:

Rather than describe all findings on each of these 6 tracings — I thought the “overall picture” conveyed by these tracings provided the more important message. Markedly increased QRS amplitude was seen in each tracing.

• Prominent J-point notching with ST elevation typical of a repolarization variant was seen in prior tracings (both of which were recorded at slower heart rates). The relative amount of inferior lead ST depression was clearly less in these earlier tracings.
• On the 4 serial ECGs recorded on this current admission — heart rate was extremely variable — slowing to ~80/minute @ 4.5 hours after admission — but increasing to a surprisingly fast 135/minute on the ECG done the next morning. The “theme” of ST-T wave appearance over the course of these 4 serial tracings — was a lessening of the ST depression, with nonspecific ST-T wave flattening in the most tachycardic tracing recorded the following morning.
• 
  
• BOTTOM Line: While possibly indicative of some ischemia — my “sum total” assessment of the 4 serial tracings from the current admission, in the context of the 2 prior tracings — was marked LVH with a repolarization variant + rate-related ST-T wave changes reflecting this patient’s evolution of his underlying medical condition — but nothing to suggest an acute cardiac event.
• 
  
• PEARL #2: Although I always advocate systematic interpretation with lead-to-lead comparison of serial ECG changes — Sometimes you just have to “stand back” from the tracings and take in the “overall theme” of what these multiple ECGs are showing. While impossible to explain the nuances of all changes on the above 6 ECGs — the “theme” is no acute OMI.

Positive Amphetamines:

While we don’t know details of this patient’s medical admission that might account for the fastest heart rate being seen on his last ECG (done the next morning) — the most plausible explanation is longterm drug abuse with acute use of amphetamines.

• Peak plasma concentration of amphetamines is rapid (within minutes) following inhalation or injection. The duration of amphetamine effect is highly variable (depending on multiple factors) — but may last hours, which may account for this patient’s labile vital signs even on the day after his admission!
• Potential cardiovascular effects of acute amphetamine use are multiple. While hypertension and sinus tachycardia are the most common manifestations — a variety of other tachyarrhythmias (including VT leading to cardiac arrest) and acute MI may be seen.
• 
  
• PEARL #3: The pathophysiologic mechanism for producing amphetamine-induced acute MI is unclear (Bazmi et al — SQUMJ 17(10); e31-37, 2017 — and — Sinha et al — Case Rep Cardiol, 2016). Possible explanations include: i) Coronary vasospasm, with a brief period of coronary occlusion; ii) Supply-demand mismatch (Type II MI) — precipitated by amphetamine-induced catecholamine surge; and/or, iii) Catecholamine-mediated platelet aggregation with subsequent thrombus formation. While OMI from acute thrombus formation is the least common of these mechanisms — acute thrombotic coronary occlusion can occur (Vichairuangthum — Arch Med Sci Atheroscler Dis 5:e45-48, 2020).

BOTTOM Line in Today’s CASE:

I was surprised by the elevated troponins in today’s case. That said — adverse effects of acute amphetamine use are well documented — and it is important to remember that acute MI from one of several potential mechanisms must be considered.

• An OMI is always a possibility with acute amphetamine use. That said — the nature of the serial ECGs in today’s case + bedside Echo that failed to show any localized wall motion abnormality excluded the need for cath lab activation in today’s case.
• In Retrospect — the marked inferior lead ST-T wave depression on the initial ECG most probably was a reflection of this patient’s Type II MI — as these inferior lead changes lessened with subsequent tracings. That said — providers were aware of the increased troponins, and clinical management throughout the case was completely appropriate.

 

A Patient with Vertigo

This patient presented with vertigo and had an ECG recorded

What do you think?

I saw this and was worried about inferior OMI due to some subtle STE in III with very worrisome reciprocal findings in aVL.  But the well-formed Q-wave and the presence of a normal T-wave in inferior leads led me to believe this was Old Inferior MI with persistent ST Elevation, otherwise known as inferior LV aneurysm.

Anterior LV aneurysm is much easier to recognize because the Q-wave is usually a QS-wave (no R-wave at all), in at least one lead.  Or at least only a very tiny r-wave (1 mm or so).

Thus, acute inferior OMI and inferior LV aneurysm is very hard to differentiate.

But the patient had previous ECGs on file from years ago, and records showed a h/o of inferior OMI with PCI:

10 years ago

This is a post PCI ECG of an inferior OMI

There are reperfusion T-waves (inverted, with well-formed pathologic Q-waves)

This previous ECG begs the question: do the upright T-waves on the presentation ECG, in contrast to the inverted T-waves on the old ECGs, represent "pseudonormalization" of T-waves, a sign of acute occlusion?

No!  Pseudonormalization can only be diagnosed in the early aftermath (days to weeks) of reperfusion.  Over time, T-waves normalize in the absence of new OMI.  So upright T-waves in the presentation ECG do NOT mean there is any re-occlusion.

5 years ago

Similar

Previous formal echocardiogram

Inferior posterior with dyskinesis

"Dyskinesis" is the technical echo term for LV aneurysm.

The combination of absence of chest pain and history of LV aneurysm made it easy to assess that this patient does not have acute OMI.

The patient ruled out by serial troponins.

I sent this ECG to the Queen of Hearts (PMcardio OMI), and here is the verdict:

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MY Comment, by KEN GRAUER, MD (7/26/2023):

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As regular followers of Dr. Smith’s ECG Blog have seen — some of the best cases that we post come from tracings that Dr. Smith or Meyers see while simply checking out “tracings on the system”. I find it especially interesting how important the History is for optimal interpretation of these cases.

• Today’s case provides perfect illustration of this observation. For clarity in Figure-1 — I’ve put the initial ECG in today’s case together with a prior tracing on the patient, done ~5 years earlier.

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NOTE: Today’s case is most insightful — IF you take another LOOK at the tracings in the sequence that Dr. Smith saw them!

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How would YOU Interpret ECG #1?

When I was given this case — I initially saw only ECG #1 — and I had not been given any clinical information.

• How would YOU interpret ECG #1 if this was the only tracing you saw — and — the only thing you knew about the patient, was that he/she was being seen in the ED?

Figure-1: Comparison of the initial ECG in today’s case — with a previous ECG recorded 5 years earlier. BUT — Please first imagine you were only given ECG #1 to look at, without the benefit of clinical information!

My Thoughts on the Initial ECG:

Systematic interpretation of ECG #1 shows:

• Sinus bradycardia at ~55-60/minute — normal intervals (PR-QRS-QTc) — normal frontal plane axis (about +20 degrees) — no chamber enlargement. 

Regarding Q-R-S-T Changes:

• Q waves — Large Q waves are seen in each of the inferior leads. A tiny q wave is seen in lead I — and narrow, but not overly deep q waves are seen in leads V5,V6.
• The QRS complex is tiny in lead V4. Given how small the QRS in this lead is — the Q wave that we see in lead V4 is disproportionately large (ie, as deep as the R wave in lead V4 is tall), wide and fragmented (ie, notched). This Q in V4 is more prominent than the narrow q waves in leads V5,V6 — which is not seen with "normal septal q waves".
• 
  
• R wave progression — Although an initial r wave is seen in lead V1 — and this r wave does become larger in lead V2 — there is loss of R wave as we move from lead V2-to-V3. We know this is not a normal finding because: i) The very next lead ( = lead V4) shows a disproportionately large and fragmented Q wave; and, ii) The initial r waves that we see in lead V1 and V2 are wider than is usually seen — and — if you look closely, the initial r waves in leads V2,V3 are also fragmented (notched).
• 
  
• ST-T waves — There appears to be subtle (minimal) ST elevation in lead III, and possibly also in lead aVF (but not in lead II). By itself — I would not know what to make of these inferior lead ST segments, as the amount of ST elevation is minimal and T waves are all upright and do not appear to be hyperacute.
• That said — there should be no doubt that the shape of the downsloping ST depression in lead aVL — and the subtly depressed flat ST segment in lead I are both abnormal. Whether this is a "new" or "old" finding is another matter.
• There are subtle-but-real ST-T wave abnormalities in the chest leads. These include: i) An upright T wave in lead V1 that is larger than the tiny upright T wave in lead V6; ii) Loss of the normal slight, upward sloping ST elevation in lead V2 (The ST segment is flat in this lead); and, iii) Disproportionately large T waves compared to the QRS in leads V3 and V4 — that may be hyperacute. 

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To EMPHASIZE: Although the amount of "words" in my above descriptive analysis is large — in practice, it literally takes me NO MORE than seconds to recognize all of these findings. The reason I continue to use this systematic checklist more than 50 years after I first began to interpret ECGs — is that this does not slow me down, while it prevents me from missing any findings.

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Putting It All Together:

How I would clinically interpret ECG #1 will depend on the History. As I stated above — I initially had no information about the patient or the clinical setting. Not knowing any clinical information about the case at the time I first saw ECG #1 — my thoughts were the following:

• Given how deep Q waves are in lead II, and especially in leads III and aVF — there has been an inferior MI at some point in time. I suspected the inferior MI was old — since the amount of ST deviation (elevation and depression) was minimal.
• There also appears to have been anterior infarction at some point in time — given "loss of R wave" (from lead V2-to-V3) + subtle-but-real fragmentation (in leads V2,V3,V4) + the disproportionately large and fragmented Q in lead V4, with tiny R wave in this lead.
• Overall — I did not get a "sense" that ECG #1 represented an acute cardiac event. That said — the T waves in lead V3 and V4 are definitely abnormal (ie, "fatter"-at-their-peak and wider-at-their-base than I would expect given modest QRS amplitude in these leads) — such that IF the history was of a patient with new-onset, worrisome chest pain — I could definitely not discount the possibility that these were hyperacute T waves.
• I thought that finding a prior ECG on this patient could prove invaluable for distinguishing between what might be "new" vs "old". Without availability of a prior tracing — I would defer my final interpretation until I had a chance to find out the clinical situation.

MORE Information is Provided!

At this point — I learned a bit more about today's patient:

• The patient is a man who had an inferior STEMI in 2010.
• He presented to the ED for today's visit because of vertigo. He did not complain of any new symptoms that might suggest an acute cardiac event.
• 2 prior ECGs were found in his medical record — the latest of which was done circa 2018 (which would be ~8 years after his inferior MI — and ~5 years before ECG #1).

To facilitate comparison in Figure-1 — I put this 2018 prior tracing ( = ECG #3) — together with ECG #1.

• The large inferior lead Q waves were present in ECG #3 — but instead of upward sloping and minimally elevated ST segments with upright T waves — ST segments were coved with T wave inversion in the inferior leads of the 2018 tracing.
• The opposite is seen for ST-T waves in high-lateral leads I and aVL, which are upright in the 2018 tracing — which is also a complete change compared to ECG #1.
• In the chest leads — QRS amplitude was much greater without Q waves, loss of R wave, or fragmentation in leads V1-thru-V4 of the prior 2018 tracing.
• The narrow q waves in leads V5,V6 are unchanged — but there is some T wave inversion in the prior tracing that is not seen in ECG #1.
• 
  
• Impression: There definitely have been changes in this patient's current ECG ( = ECG #1) — compared to his prior tracing from 2018. Evidence of the 2010 inferior infarction (in the form of large inferior Q waves) is present in both ECG #1 and ECG #3. I thought the deep S waves in leads V1,V2 with associated ST-T wave changes may have represented LVH on the 2018 tracing. In between the time from 2018 until the current tracing was recorded — the current ECG suggests there has been anterior infarction.
• In view of the History with the current admission (ie, presenting to the ED for vertigo — with no new chest pain) — I interpreted ECG #1 as no OMI.
• 
  
• Follow-Up: Cardiac troponins were negative — ruling out an acute event.

FINAL Thoughts:

• Optimal clinical ECG interpretation is impossible in the absence of a brief, relevant history.
• We know today's patient had a documented inferior STEMI in 2010. Comparison of present and prior ECGs suggest that the patient has also had an anterior infarction since 2018.
• It will be important for optimal longterm clinical management of this patient to figure out what happened when — but this is not yet possible from the limited information we have available. Close follow-up will be essential — but there was no acute OMI today ...