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).