Chest pain: Are these really "Nonspecific ST-T wave abnormalities", as the cardiologist interpretation states?

Written by Jesse McLaren, with a very few edits by Smith

 

A 60-year-old presented with chest pain. The ECG did not meet STEMI criteria, and the final cardiology interpretation was “ST and T wave abnormality, consider anterior ischemia”. But are there any other signs of Occlusion MI?

There’s only minimal ST elevation in III, which does not meet STEMI criteria of 1mm in two contiguous leads. But STEMI criteria is only 43% sensitive for OMI.[1] But there are multiple other abnormalities that make this ECG diagnostic of Occlusion MI, localized likely to the right coronary artery:

1. AV block, which can be a transient complication of RCA occlusion since it perfuses the AV node [2]

2. Inferior hyperacute T waves, which have been added to the 2022 ACC consensus on chest pain as a “STEMI equivalent”[3]

3. Reciprocal ST depression and T wave inversion in aVL, which is 99% sensitive for inferior OMI.[4]

4. Ischemic ST depression V2-4, which is 97% specific for posterior OMI[5]

 

So this patient with chest pain has an ECG that is diagnostic of inferior and posterior OMI complicated by 3^rd degree AV block, likely representing an RCA occlusion. (See Ken Grauer discussion below for more on AV blocks in today's case).

These findings are diagnostic even without comparison with an old ECG.  

But they are even more striking when you do compare with the old one: 

Here’s a side-by-side comparison of the inferior leads from the baseline ECG (left) and new ECG (right) showing hyperacute T waves with reciprocal change in aVL:

The hyperacute T waves are not tall in absolute terms (only 4mm) but they are tall relative to the QRS, broad based, bulky and look inflated. The T wave inversion in aVL is not necessarily abnormal because it is concordant with the negative QRS, but it is huge relative to the QRS, reciprocal to the hyperacute T wave in III

The ECG also shows how reciprocal change can be the more obvious finding of OMI. Here are leads aVL and V2 of the new ECG, flipped upside down:

 

With the leads flipped, aVL has an obvious hyperacute T wave larger than the entire QRS complex, while V2 has ST elevation.

If simply flipping leads upside down can show signs of occlusion, then there’s a problem with a paradigm that dichotomizes ST segment deviation between elevation and depression as seen on the ECG paper, because they can reflect the same current of injury in the patient from a different view.[6] When there’s a current of injury towards a territory it produces reciprocal change in its wake, which is sometimes more obvious than the territory of injury (for inferior OMI) and is sometimes the only sign on the 12 lead (for posterior OMI). AVL and V2-V3 are oriented to reflect the reciprocal change to inferior and posterior OMI respectively – but this helpful information is disregarded by STEMI criteria because these leads manifest ST depression instead of ST elevation. Hence the first ECG was labeled 'anterior ischemia' based on ST depression, rather than identifying this as reciprocal from posterior OMI.

 

With a “STEMI negative” ECG and ongoing chest pain, the ECG was repeated in 10 minutes:

Now the AV block has improved from 3^rd to 1^st degree. But there are ongoing inferior hyperacute T waves, reciprocal TWI in aVL, and ischemic STD in V2-3. The final interpretation is now “nonspecific ST abnormality” based on STEMI criteria, but it is still very specific for infero-posterior OMI. There’s also more greater reciprocal change - here’s aVL flipped, with a T wave that now towers over the tiny QRS:

But now the patient has now had serial ECGs which are “STEMI negative”. So a troponin level was sent: 90 minutes later it returned at 250ng/L (normal <26 in males and <16 in females). Then the ECG was repeated again:

Now the ECG just barely meets STEMI criteria, along with more obvious hyperacute T waves.

A 15 lead was done 7 minutes later:

Now greater inferior ST elevation, and some convex ST segment in V5-6. Posterior leads V8-9 are also elevated, but this only confirms the posterior OMI that was seen on the first ECG.

Here’s a view of the last ECG showing V2-3 flipped (on the left) compared with V8-9 (right) :

The flipped V2-3 show clear ST elevation and hyperacute T waves, while V8-9 have lower voltage and proportionally less obvious ST/T changes which add no additional value.

Since the ECG now meets STEMI criteria, a code STEMI was activated. There was a 99% mid RCA occlusion, and peak troponin was greater than 25,000ng/L (upper limit of assay). 

Discharge ECG showed resolution of changes, and subtle inferior reperfusion T wave inversion:

This patient received the standard of care under the current STEMI paradigm: serial ECGs for ongoing chest pain, and waiting for troponin level for "STEMI negative" ECGs. But this led to a 90 minute delay to reperfusion for an occlusion that could have been identified on the first ECG. This is typical of the current paradigm, as OMI findings can identify occlusions a median of 1.3 hours earlier.[7] 

Earlier intervention could have saved myocardium possibly a huge amount of myocardium, and could easily have been done if the mind set and approach was OMI-NOMI rather than STEMI/NSTEMI and if the Queen of Hearts app was used.

 

There is now AI trained to identify OMI.[8] If this been available in this case, the diagnosis could have been made on the first ECG, and saved 90 minutes of reperfusion delay. 

Here’s the Queen of Heart’s interpretation on the first ECG, along with explainability:

Even without comparison to the prior, and without any reference to the minimal ST elevation in III, the Queen identifies OMI with high confidence based on inferior hyperacute T waves, reciprocal T wave inversion in aVL, and anterior ST depression. She is not bothered by lead orientation, and is equally comfortable identifying OMI by the reciprocal hyperacute T waves or in the reciprocal ST depression.

Click here to sign up for Queen of Hearts Access

 

Take away

1. STEMI criteria misses the majority of OMI, and leads to delayed reperfusion for STEMI(-)OMI

2. Findings of RCA occlusion may include AV block, subtle inferior ST elevation, hyperacute T waves, reciprocal STD/TWI in aVL, and anterior STD from associated posterior OMI

3. Reciprocal change can be more obvious than the primary injury, and posterior leads rarely add any additional value to the ischemic STDmaxV1-4 that can be seen on 12 lead

4. OMI ECG findings can lead to rapid diagnosis, and can be widely disseminated through AI

 

References

1. De Alencar Neto. Systematic review and meta-analysis of diagnostic test accuracy of ST-segment elevation for acute coronary occlusion. Int J Cardiol 2024

2. Nikus et al. Conduction disorders in the setting of acute STEMI. Curr Cardiol Red 2021

3. Kontos et al. 2022 ACC expert consensus decision pathway on the evaluation and disposition of acute chest pain in the emergency department: a report of the American College of Cardiology solution set oversight committee. J Am Coll Cardiol 2022

4. Bischof et al. ST depression in lead AVL differentiates inferior ST-elevation myocardial infarction from pericarditis. Am J Emerg Med 2016

5. Meyers et al. Ischemic ST-segment depression maximal in V1-4 (versus V5-6) of any amplitude is specific for occlusion myocardial infarction (versus nonocclusive ischemia). J Am Heart Assoc 2021

6. Phibbs and Nelson. Differential classification of acute myocardial infarction into ST- and non-ST segment elevation is not valid or rational. Ann Noninvasive Electrocardiol 2010

7. Meyers et al. Accuracy of OMI ECG findings versus STEMI criteria for diagnosis of acute coronary occlusion myocardial infarction. IJC Heart and Vasc 2021

8. Herman et al. International evaluation of an artificial intelligence-powered electrocardiogram model detecting acute coronary occlusion myocardial infarction. Eur Herat J Digital Health 2024

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MY Comment, by KEN GRAUER, MD (5/27/2024):

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Superb presentation by Dr. McLaren on a case that clearly could have been (should have been) diagnosed as acute infero-postero OMI based on the initial ECG.

• The fact that this ECG was initially diagnosed as showing, “ST-T wave abnormality — consider anterior ischemia” — means that the provider failed to recognize the AV block. The reason this happens is simply because of a failure to spend the 2-3 seconds it takes for an ‘educated eye” to routinely scan the long lead II rhythm strip, looking to see if there are upright P waves that precede each QRS complex with a fixed PR interval. Try this. Isn’t it easy to see in no more than 2-3 seconds that regular P waves do not precede each QRS with a fixed PR interval in today’s initial ECG?
• 
  
• PEARL: If you do not want to overlook 2nd- and 3rd-degree AV Blocks — Make it a habit as soon as you are given any ECG to always spend your first 2-3 seconds (which is all it should take) ensuring that P waves are present and are (or are not) related to neighboring QRS complexes. 
• As per Dr. McLaren — the rhythm in today’s initial ECG is 3rd-degree ( = complete) AV Block — here at the AV Nodal level, given the narrow QRS complex of ventricular beats at an escape rate ~50/minute (well within the 40-60/minute usual range for AV nodal escape).
• PEARL: In my experience — the BEST clue to distinguish 2nd-degree from 3rd-degree AV block — is that most of the time with 3rd-degree, the ventricular response will be regular. This is because most of the time escape rhythms are regular (or at least fairly regular). IF instead of being regular — you see a ventricular beat that clearly occurs earlier-than-expected — the chances are that the degree of AV block is not complete.
• The initial ECG in today’s case is complete AV Block beause: i) The atrial rhythm is quite regular; ii) The ventricular rhythm is quite regular; and, iii) P waves are not related to neighboring QRS complexes (ie, P waves “march through the QRS complexes” — which is easily established by noting the constantly changing PR interval) — and, iv) No P waves are conducted despite having adequate chance to do so (ie, While in today’s initial ECG, we would not expect those P waves with a short PR interval to conduct — there is more than adequate opportunity for those P waves occurring in the middle of the R-R interval to conduct in this tracing, yet they fail to do so).
• As per Dr. McLaren — it is common to see AV Block in patients with acute inferior, posterior and/or infero-postero OMI. The “culprit” artery will almost always be either the RCA or LCx, as either vessel may supply the AV node (the “culprit” being the RCA in today’s case). PEARL: Even if providers failed to appreciate the diagnostic features of acute infero-postero OMI in today’s initial ECG —The failure to spend those 2-3 seconds surveying the long lead II rhythm strip should have prompted recognition that the chest lead ST-T wave depression was unlikely to be the result of “anterior ischemia” — and much more likely to reflect acute infero-postero OMI — since 2nd- and/or 3rd-degree AV block with a narrow QRS is common with infero-postero OMI — but it is rare with anterior ischemia/OMI.
• 
  
• PEARL: When AV block with a narrow QRS occurs in association with acute inferior and/orposterior OMI — there is often a step-wise progression and/or regression (ie, from 1st-degree — then to 2nd-degree, Mobitz Type I — then to 3rd-degree AV block at the AV nodal level — or — from 3rd-degree — to Mobitz I 2nd-degree — to 1st-degree, IF the patient began with complete AV block). As per Dr. McLarren, the “good news” — is that most of time, the associated AV block will resolve, especially if there is prompt reperfusion of the “culprit” artery.

Playing “Devil’s Advocate”: In view of this last Pearl — I suspect that the 2nd ECG in today’s case (done just 10 minutes after the 1st ECG) represents 2nd-degree 2:1 AV Block of the Mobitz I Type — and not just sinus rhythm with 1st-degree AV Block.

• We often see both 1st-degree AV block (ie, of conducted beats) — and 2nd-degree Mobitz I AV block together!
• The atrial rate in today’s 1st ECG is just under 100/minute — and the junctional escape rate is ~50/minute.
• The ventricular rate remains the same ~50/minute in the 2nd ECG — but for this to be sinus rhythm with 1st-degree, the atrial rate would have to have decreased from just under 100/minute to 50/minute over a 10-minute period.
• The very subtle “extra” widening of the T wave peak in the inferior leads, and of the inverted T wave in lead aVL occurs at an appropriate moment in the R-R cycle to potentially “hide” a 2nd P wave (especially if there is some ventriculophasic sinus arrhythmia — as there so commonly is with 2nd-degree AV block). And, if a 2nd P wave is “hiding” within each T wave — this would represent an atrial rate that is still just under 100/minute — instead of having to postulate that the atrial rate so rapidly decreased to ~50/minute.
• The atrial rate in the 3rd ECG is clearly much faster than 50/minute.
• And, the reason I so carefully considered the possibility of 2:1 AV block in today’s 2nd ECG — is that as per the above Pearl, it is common for 3rd-degree AV block at the AV Nodal level to resolve with stepwise regression (ie, passing from 3rd-degree — to 2nd-degree, Mobitz I — and then to 1st-degree, before finally returning to normal sinus conduction).
• 
  
• To EMPHASIZE: I can not prove whether or not my suspicion that the 2nd ECG in today’s case represents 2:1 Mobitz I instead of sinus rhythm with 1st-degree.  To prove this — I’d need to see serial ECG monitoring revealing what happens with respect to the atrial and ventricular rates as the case evolves.
• That said — Clinically, it does not matter if the 2nd ECG shows sinus rhythm at ~50/minute with 1st-degree vs Mobitz I 2nd-degree with 2:1 AV block and 1st-degree — because the ventricular rate is the same in either case and chances are that the AV block will resolve with treatment.
• 
  
• PEARL: The above said — there are times when it will matter clinically whether your patient with acute infero-postero OMI is in sinus rhythm vs 2nd-degree, Mobitz I with 2:1 AV block (in which the 2nd P wave is hidden within T waves). Awareness of when and how to look for 2:1 block in subtle cases (as I describe above for today’s 2nd ECG) can greatly facilitate identification.

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ADDENDUM (5/28/2024):

I wrote the above comment yesterday — while traveling, without large screen computer and without calipers.

• To EMPHASIZE: Calipers were not needed to optimally treat the patient in today's case — as Dr. McLaren superbly demonstrates in his discussion. But I find it helpful after the emergency has passed to reflect on events for my own edification — so that I can learn and do even better in the future.
• 
  
• The above said — After returning home and able to view these 2 ECGs better — it literally took me no more than seconds using calipers to verify what took so much longer without them.

I've labeled the first 2 ECGs in today's case in Figure-1.

• RED arrows make the ventriculophasic sinus arrhythmia obvious in ECG #1. Of note — most of the time when ventriculophasic sinus arrhythmia is seen in AV block rhythms — it is the P-P interval that "sandwiches" the P wave that is shorter (thought to be due to transient increased perfusion from the QRS) — but we see the opposite in Figure-1.
• Complete AV block (as per Dr. McLaren) is clearly present in ECG #1 (quite regular junctional escape — but absolutely no relation between the sinus arrhythmia and neighboring QRS complexes despite adequate opportunity to conduct).
• 
  
• Impossible to prove anything in ECG #2, because there is no long lead rhythm strip — but the PINK arrows suggest ever-so-subtle deflections that I suspect represent "hidden" P waves from regression of 3rd-degree — to 2nd-degree AV block, Mobitz Type I with 2:1 AV conduction in this repeat ECG done 10 minutes after ECG #1.

Figure-1: I've labeled the 1st 2 ECGs in today's case.

Is this Rhythm Puzzling to You?

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My Comment by KEN GRAUER, MD (3/30/2023):

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The ECG in Figure-1 was sent to me without the benefit of any history. I thought the rhythm illustrated a number of essential concepts for clinicians dedicated to Emergency Care.

• Do YOU know what the rhythm is?
• 
  
• IF this arrhythmia is puzzling to you — READ ON!  I illustrate how to make the diagnosis within less than 15 seconds.

Figure-1: The initial ECG in today's case. This tracing was sent to me without the benefit of any history. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Initial Thoughts on the ECG in Figure-1:

As noted — I was sent today's ECG without the benefit of any history, other than knowing that the patient presented to the ED. 

• My quick initial survey of this tracing revealed T wave inversion in lead aVL and some T waves that might be hyperacute (ie, in the inferior leads and in V1,V2,V3). That said, although this ECG is suspicious — I thought it was not at this point diagnostic of acute OMI. 
• Clinically — Since this ECG is not at this point diagnostic — whether or not an acute cardiac event was in progress would appropriately be delayed until some history, a repeat ECG, and troponins could be obtained. In the meantime — I focused my attention on the "eye-catching" arrhythmia in the long lead II rhythm strip.

Time-Efficient Assessment of Today's Rhythm:

Once you ensure that the patient is hemodynamically stable — I favor the systematic Ps, Qs, 3R Approach for rhythm assessment (Are there P waves? — Is the QRS wide or narrow? — and the Rate and Regularity of the rhythm? — and whether P waves are Related to neighboring QRS complexes?):

• To Emphasize: It does not matter in what sequence you assess the Ps, Qs & 3Rs. I favor starting with whichever of these 5 parameters are easiest to assess.
• The QRS is narrow in all 12 leads of today's tracing. This tells us that the rhythm is supraventricular.
• P waves are present! (RED arrows in Figure-2 highlight those P waves that we can easily identify).
• The ventricular rhythm is not Regular! That said — there is a "pattern" to the rhythm in Figure-2 — in that there is group beating in the form of a "bigeminal" rhythm, with groups of shorter-then-longer R-R intervals (horizontal BLUE lines in Figure-2 facilitating recognition of groups with the shorter R-R interval).
• As to the atrial and ventricular Rates — these vary in Figure-2, because of the irregularity of the rhythm, but neither the atrial nor ventricular rates appear to be excessively fast.
• 
  
• The last parameter in my systematic Ps, Qs, 3R Approach — is the 3rd "R" — which asks the question of whether atrial activity is Related to neighboring QRS complexes?
• 
  
• KEY Question: Look in Figure-2 at the RED-arrow P waves in front of each QRS complex that ends a longer R-R interval (ie, Look at the PR intervals for the RED-arrow P waves in front of beats #1, 3, 5, 7 and 9). Although greatly prolonged (to a PR interval ~0.46 second) — Aren't each of these PR intervals the same? 
• 
  
• 
  
• ANSWER: The fact that the PR interval in front of each of the odd-numbered beats in Figure-2 is the same tells us that these P waves are being conducted to the ventricles! (albeit with marked 1st-degree AV block).

Figure-2: I've labeled with RED arrows those P waves we can definitely identify. In addition — there is group beating (with horizontal BLUE lines facilitating recognition of groups with the shorter R-R intervals).

Is the Atrial Rhythm Regular? 

• In Figure-2 — I highlighted with RED arrows those P waves we could be certain about. Rather than the "grouped beating" of P waves suggested by these RED arrows — Wouldn't it be much more logical for the underlying atrial rhythm to be regular? — with additional "on-time" P waves being hidden within the QRS complex of beats #2, 4, 6, 8 and 10 (PINK arrows in Figure-3)?
• 
  
• Technical NOTE (Beyond-the-Core): It is not possible to "prove" that the PINK arrows in Figure-3 truly represent P waves because: i) There is an underlying sinus arrhythmia — with slight variation in the P-P interval of the RED arrows in Figure-2; and, ii) There is slight variation in QRS morphology for every-other-beat in Figure-2 — which makes it impossible to tell if this change in the QRS morphology of all even-numbered beats is purely the result of aberrant conduction — or — whether there might also be some hidden deformation of the QRS of beats #2,4,6,8,10 by hidden P waves.
• 
  
• PEARL #1: Common things are common! It is far more likely for the atrial rhythm in Figure-3 to be regular (or at least almost regular — with slight variation due to sinus arrhythmia) — than for there to be the rare rhythm of atrial parasystole with 3:2 exit block. Atrial bigeminy (ie, every-other-P wave being a PAC) is unlikely in Figure-3 — because P wave morphology under each of the RED arrows in Figure-3 looks so similar (whereas P wave morphology usually is noticeably different with PACs).

Figure-3: I've labeled with PINK arrows the likely location of hidden "on-time" P waves. Isn't it likely that the underlying atrial rhythm is regular?

Putting It All Together:

By the Ps, Qs, 3R Approach — we have determined the following for the rhythm in Figure-3:

• The rhythm is supraventricular (all QRS complexes are narrow — albeit with slight variation in QRS morphology every-other-beat due to some aberrant conduction).
• There is group beating (alternating shorter-then-longer R-R intervals).
• The atrial rhythm is essentially regular (with slight variation in the P-P interval due to some sinus arrhythmia). That said — there are more P waves than QRS complexes — so at least some of these on-time P waves are not being conducted.
• That said — the PR intervals for the RED-arrow P waves in front of each odd-numbered beat (ie, in front of beats #1,3,5,7,9) are equal! This proves that at least these beats are conducting.

PEARL #2: The above characteristics overwhelmingly point to AV Wenckebach (ie, 2nd-degree AV block, Mobitz Type I ) as the etiology of today's rhythm!

• To Emphasize: Although my above description may seem to be in "slow motion" — I literally knew within seconds that today's rhythm was almost certain to represent some form of AV Wenckebach because: i) There is group beating (which the "trained eye" should instantly recognize); ii) The atrial rhythm is almost regular ( = sinus arrhythmia, which with use of calipers is literally established within seconds); and, iii) The 1st beat in each group is conducting (witness the repeating equal PR interval in front of beats #1,3,5,7,9); and, iv) There is 1st-degree AV block (It is very common for conducted beats with AV Wenckebach to manifest 1st-degree block).  

Looking CLOSER at the Rhythm:

The reason today's rhythm is challenging — is that the 1st conducted beat in each grouping has a very long PR interval. To facilitate recognition of each 3:2 Wenckebach cycle — I have chosen a different color for each P wave (Figure-4).

• As already stated — RED-arrow P waves represent conduction of the 1st beat in each group with a long PR interval ( = 0.46 second). 
• The YELLOW-arrow P waves in each group are not conducted. (This makes sense — because these YELLOW P waves are simply not in a position where conduction is possible).
• 
  
• By the process of elimination — the BLUE-arrow P waves must therefore be conducting. That this is the case is supported by the fact that all PR intervals from a BLUE arrow until beats #2,4,6,8 and 10 are equal (albeit very long = 0.64 second). So — this is AV Wenckebach with 3:2 AV conduction (as the PR interval within each group increases from 0.46 second — to 0.64 second — until the YELLOW-arrow P waves are non-conducted).

Figure-4: Colored arrows facilitate recognition of PR interval prolongation (from RED arrow P waves that conduct with a PR interval = 0.46 second — to 0.64 second for BLUE arrow P waves) — until non-conduction of the YELLOW arrow P waves.

LADDERGRAM Illustration:

• Doesn't the laddergram in Figure-5 clarify the mechanism of today's rhythm?

Figure-5: Laddergram illustration of today's rhythm.

Final POINTS:

• It is extremely common to see slight variation in the P-P interval in association with either 2nd- or 3rd-degree AV block. This is known as a "ventriculophasic" sinus arrhythmia — with the theory being that the P-P interval may vary because of improved coronary perfusion, depending on whether mechanical contraction (signaled by electrical activity from a QRS) is "sandwiched" between 2 P waves.
• Mobitz I 2nd-degree AV Block (ie, AV Wenckebach) — is very commonly associated with acute inferior infarction. IF you return for a moment to the 12-lead ECG shown in Figure-1 — I was concerned when I first saw this tracing that the T wave inversion in lead aVL — and the hypervoluminous T waves in the inferior leads and in V1,V2,V3 might be markers of a recent inferior OMI? While I did not think the initial ECG in Figure-1 was diagnostic — I felt additional information (ie, some history, repeat ECGs, troponin) was clearly indicated to clarify the clinical situation. Unfortunately — we are not privilege to the clinical outcome in today's case.

And 3 Advanced Concepts ...

• As alluded to earlier — the 2nd beat in each group is slightly wider and slightly different in morphology from the 1st beat in each grouping. This is most probably the result of aberrant conduction by the Ashman phenomenon (ie, The slightly longer R-R interval between beats #2-3; 4-5; 6-7; and 8-9, may prolong the relative refractory period of the next beat = of beats #3,5,7,9 — which results in aberrant conduction of beats #4,6,8,10).
• Another reason today's rhythm is challenging to interpret — is that the PR interval "increment" (ie, The amount that the PR interval is increased from 1 beat to the next within a Wenckebach cycle) — is much more than usual (ie, The PR interval increases from 0.46-to-0.64 second). While this might simply be the result of an atypical Wenckebach — it might alternatively reflect dual AV nodal pathways, each with its own degree of impaired conduction.
• Finally — The fact that the PR interval for conducted beats in today’s tracing is very long may of itself be of clinical significance. This is because once the PR interval extends beyond ~0.30 second — the delay in ventricular contraction that occurs may result in the atria contracting against closed AV valves, with reduction in cardiac output. Thus, although Mobitz I is often a well tolerated rhythm — that may not necessarily be the case in today's tracing (especially if it did turn out that this patient had a recent inferior infarction).

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For Readers Wanting More ...

For readers in search of additional practice of concepts from today's case — I refer you to My Comment in the following posts in Dr. Smith's ECG Blog:

• The May 16, 2020 post.
• The January 26, 2023 post.
• The August 17, 2020 post.
• The March 14, 2022 post.

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A man in his 40s who really needs you to understand his ECG

 Written by Pendell Meyers

A man in his 40s presented for "left sided chest pain sudden onset yesterday when sneezing and coughing that is worsened with inspiration." He also complained of associated SOB, dizziness, jaw pain, and back pain, which he described as "muscle spasms." He has also had rhinorrhea and cough for 1 week. Also, left hand numbness today. 

He went to urgent care for evaluation. An ECG was performed there (unavailable) which reportedly was abnormal, so EMS was called to urgent care to take him to the ED.

On EMS arrival, they noted the patient vomited then became unresponsive. He was reportedly in PEA arrest, so they started chest compressions. After approximately 30 seconds of compressions, before the defibrillator could be applied, the patient started moving and moaning. Vitals then showed bradycardia, hypotension, and hypoexmia. He was then transported to the ED.

EMS recorded an ECG and transmitted it to the ED physicians before arrival:

Here is the same image after PM Cardio app processing:

What do you think?

It's an unusual and terrifying ECG. There is sinus rhythm at a rate of approximately 120 bpm with 2:1 AV block (see lead V1 where the P waves are very clear), resulting in ventricular rate near 60 bpm. The QRS shows RBBB and LAFB. There is concordant STE in V1-V5. The inferior leads have large upright T waves that are likely hyperacute, with reciprocal large volume TWI in aVL (these are more than expected for the LAFB). The T waves in V2-V4 have terminal T wave inversion, but I am not convinced or reassured that there might be meaningful reperfusion; overall it looks like active OMI.

In other words, it is diagnostic for proximal LAD occlusion (or even left main), but with the addition of 2:1 AV block. 

First ECG on ED arrival:

Similar to EMS ECG.

20 min later:

Mostly similar to above.

The cath lab was activated.

Bedside echo showed very poor LV function, diffuse bilateral B lines. The ED physician diagnosed cardiogenic shock from OMI.

The cardiologist cancelled the cath lab activation and presented to bedside. He stated that he would not cath the patient before PE was ruled out by CT angiogram.

Side note: Even without understanding the ECG, PEs do not usually cause acute AV block, and obviously the ED bedside echo is the opposite of RV failure. 

The ED provider was unable to convince him otherwise, so rolled the patient immediately to CT and performed CT angiogram within 20 minutes, and convinced the cardiologist that there was no large proximal PE on the scan.

And so the delay to cath was only about 45 minutes or an hour. At cath, the patient's cardiac index was 1.9 L/min/m2 even on dopamine, and an impella assist device was placed prior to angiogram. He was also intubated around this time.

Angiogram showed acute thrombotic 100% occlusion of the proximal LAD. The report also describes 100% stenoses at the mid and distal LAD. Three stents were placed, in the prox, mid, and distal LAD. In each location, the residual stenosis is listed at 0%. Unfortunately, the post procedure TIMI flow is listed as 2 (instead of 3, which would be normal flow and successful reperfusion). There is no description in the cath report detailing the reasons and attempted interventions for suboptimal flow, unfortunately. I get the sense that, despite best efforts, flow through the culprit LAD was unable to be perfectly restored despite PCI.

Here are some of the cath images:

Pre-intervention. Red arrows show the location of the proximal LAD Occlusion.

Post-intervention. Even after waiting several seconds since contrast infusion to capture the image, you can see the LAD is not fully perfused with contrast even when the other visible vessels are. In video, the contrast creeps very slowly past the original lesion and down the LAD. 

There is no post cath ECG immediately available.

Initial troponin T (older generation, both limit of detection and lowest abnormal value is 0.01 ng/mL; in other words, the assay is either undetectable at less than 0.01 ng/mL, or abnormal at 0.01 or above) returned at 4.52 ng/mL (very high, already higher than the average STEMI in our studies).

Later that night, this occurred (pt intubated, sedated):

Two of the P waves conduct, otherwise this is complete AV block with resultant ventricular asystole.

Transcutaneous pacing ensued, then a transvenous pacemaker was placed (it seems that 2:1 AV block had not been noticed on prior ECGs, and no temporary pacer wire was placed during the cath lab!).

Here is the ECG after TVP:

Ventricular paced rhythm. Use the modified Sgarbossa criteria and tell me: is there evidence of downstream reperfusion after PCI?

Here are a few leads blown up:

Here they are annotated for the ST/S ratios we use in the modified Sgarbossa criteria:

As you can see, the ECG is positive for the modified Sgarbossa criteria, suggesting ongoing evolution of OMI. The inferior leads also look concerning. Notice that the ECG is falsely negative for OMI by the original Sgarbossa criteria, as there is no lead with 5mm of discordant STE.

Sadly, this is worrisome for no-reflow phenomenon. Despite the intervention improving angiographic flow, the myocardium does not show signs of meaningful reperfusion. Instead, the ECG is playing out as a full thickness completed MI.

Poor Microvascular Reperfusion ("No Reflow"): Best Diagnosed by ECG

Echo the next morning showed EF 24% with severe hypokinesis of the anterior, anterolateral, mid inferior, basal anterior septum, mid inferior septum, and the entire apex. There was also severe swirling of contrast in the LV apex consistent with low flow state. There was a very tiny thin mobile echodensity seen attached to the apical lateral wall, which may represent LV thrombus.

Troponin T peaked at 8.43 ng/mL (very high, terrible MI and long term outcome).

Days later:

RBBB with anterior LV aneurysm morphology. 

[There are QR-waves with shallow T-wave inversion -- LV aneurysm usually has QS-waves, but QS-waves become QR-waves in the setting of RBBB].  
See this post: Dyspnea, Right Bundle Branch block, and ST elevation

The patient apparently survived to discharge, but long term follow up is obviously bleak.

Learning Points:

Acute ACS with new RBBB and LAFB is a very high risk sign of proximal LAD OMI, with very high rates of cardiogenic shock and death even before emergent intervention.

PE doesn't cause AV block.

Use the modified Sgarbossa criteria as the best available approach to finding OMI in ventricular paced rhythm.

No reflow phenomenon occurs when microvascular reperfusion fails despite epicardial coronary intervention. It cannot be predicted before attempting intervention as far as I know.

Other cases of LAD OMI with RBBB/LAFB:

Cardiac Arrest at the airport, with an easy but important ECG for everyone to recognize

A woman in her 60s with 6 hours of chest pain, dyspnea, tachycardia, and hypoxemia

Ventricular Fibrillation, ROSC after perfusion restored by ECMO, then ECG. Protocols can be overridden by Physician Judgment.

What is the Diagnosis in this 70-something with Chest Pain?

68 minutes with chest compressions, full recovery. Plus recommendations from a 5-member panel on cardiac arrest.

A deadly alcohol binge: a man in his 30s with chest pain and initial high sensitivity troponin I within normal limits

Wide Complex Tachycardia; It's really sinus, RBBB + LAFB, and massive ST elevation

Resuscitated from ventricular fibrillation: what is the ECG Diagnosis?

A man in his 80s with chest pain

What, besides large anterior STEMI, is so ominous about this ECG?

Chest Pain and Right Bundle Branch Block

Some of the most severe LAD or left main occlusions present with acute RBBB and LAFB, and these findings carry the highest risk for acute ventricular fibrillation, acute cardiogenic shock, and highest in-hospital mortality when studied by Widimsky et al. (in-hospital mortality was 18.8% for AMI with new RBBB alone). Additionally, the RBBB and LAFB make the recognition of the J-point and STE more difficult and more likely to be misinterpreted. Upon successful and timely reperfusion, the patient may regain function of the previously ischemic or stunned fascicles.

Widimsky PW, Rohác F, Stásek J, et al. Primary angioplasty in acute myocardial infarction with right bundle branch block: should new onset right bundle branch block be added to future guidelines as an indication for reperfusion therapy? Eur Heart J. 2012;33(1):86–95. 

https://pubmed.ncbi.nlm.nih.gov/21890488/

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MY Comment by KEN GRAUER, MD (5/1/2022):

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Highly instructive case presented by Dr. Meyers — with a series of lessons to remember. I focus my comments on the processed PM Cardio app version of the initial EMS tracing, that I’ve reproduced in Figure-1.

As per Dr. Meyers — this ECG is highly suggestive of acute proximal LAD occlusion. It does not suggest acute PE.

• There is bifascicular block (RBBB/LAHB) — which is a common accompaniment of large proximal LAD occlusions.
• The usual initial positive deflection (r wave) of RBBB has been replaced by large initial Q waves in leads V1 and V2 (confirming the large anteroseptal infarction). The extra fragmentation (notching) in lead V2, and especially in leads V3,V4 — provides additional evidence of “scar”.
• Support that the LAD occlusion begins proximally — is forthcoming from the finding that ST elevation begins immediately with lead V1. ST elevation appears to be maximal in leads V3,V4 — and continues through to lead V5.

PEARL #1: Normally with complete RBBB — there will be a certain amount of ST-T wave depression in this lead, reflecting the oppositely-directed repolarization change expected with RBBB. The fact that despite this, there still is some ST elevation in lead V1 suggests that were it not for this conduction defect — the relative amount of ST elevation in lead V1 would have been significantly greater.

• NOTE: Concern was voiced by Cardiology regarding the possibility of a large acute PE. While anterior T wave inversion with a long QTc are findings that suggest acute RV “strain” —  the rest of the 12-lead (as per Dr. Meyers), is not suggestive of acute PE because: i) The presence of AV block (See below); ii) The ST elevation that is seen in leads V1-thru-V5 (which is not expected with acute PE); and, iii) An ST-T wave appearance in the inferior leads that is the complete opposite of what should be expected with a large acute PE (ie, hypervoluminous, hyperacute-appearing T waves in the inferior leads — instead of the T wave inversion of RV strain).

Figure-1: The processed PM Cardio app version of the initial EMS tracing.

What About the Rhythm in Figure-1?

It would be easy to misdiagnose the rhythm in Figure-1 as sinus. This is because the long lead II rhythm strip that appears at the bottom of the 12-lead “looks like” a simple sinus rhythm at a seemingly reasonable rate just under 60/minute. But as Dr. Meyers points out — instead of sinus rhythm, there is 2:1 AV block.

• Note first that the long lead II rhythm strip in this EMS tracing is not simultaneously recorded with the rest of the ECG. Recognition of this fact is important — because it means that we can not correlate the timing of certain deflections that we see in other leads with what is happening in the long lead II rhythm strip.
• In general, the best lead for identifying P waves in, is standard lead II. Lead II provides the extra advantage of verifying a sinus mechanism if the P wave in this lead is upright. In my experience — the 2nd-best lead for identifying P waves in is lead V1. The interesting feature about the rhythm in this initial EMS tracing — is that the hypervoluminous T wave in lead II is “hiding” the extra P wave (PINK arrows in the long lead II). This would have been extremely to miss if the search for atrial activity only included a look at lead II.

Lead V1 provides the answer — with RED arrows in this lead highlighting 2:1 AV conduction. Support that the “extra deflection” within the R-R interval in lead V1 is truly an extra P wave (and not artifact or some unusual form of T wave notching) — is forthcoming from: i) The unique biphasic (positive-then-negative) shape of the deflections under the RED arrows; ii) The almost-equal distance between these deflections (ie, PACs would not be so equi-distantly placed); and, iii) The fact that we can see a similarly placed extra deflection in simultaneously-recorded leads V2 and V3 (although the extra P waves are even more subtle in those leads).

• I believe the reason the 2:1 block in this tracing is so challenging to recognize, is due to a combination of: factors. These include: i) The rapid atrial rate (ie, ~115-120/minute) — which results in the extra T wave occurring so early in the cardiac cycle; ii) The hypervoluminous inferior lead T waves (as a result of the acute OMI) which facilitate the “hiding” of the extra P wave; and, iii) The “ventriculophasic” sinus arrhythmia. 

PEARL #2: Be aware that ventriculophasic sinus arrhythmia is commonly seen with 2nd- and 3rd-degree AV blocks. In its typical form — it is the P-P interval that “sandwiches” a QRS complex that measures slightly less than the P-P interval without any QRS within it, as is seen in Figure-1 (ie, 510 msec. compared to 530 msec.). 

• It is thought that the reason for slight shortening of the P-P interval for P waves that sandwich a QRS — is that mechanical (ventricular) contraction follows soon after electrical activity (ie, the QRS) — and this results in slightly improved blood flow (therefore, slight shortening of the P-P interval).

PEARL #3: How NOT to Miss AV Block:
As emphasized — the 2:1 AV block in today’s initial tracing is challenging to recognize! That said — there are some easy things to do that will minimize the chance of overlooking subtle arrhythmias like this one.

• Increase your index of suspicion for a rhythm disorder when you encounter a predisposing clinical setting. The patient in today’s case had just survived a cardiac arrest. His initial ECG showed bifascicular block (presumably new) — in association with acute ST-T wave changes suggestive of LAD occlusion. In this setting — I would not have expected a simple sinus rhythm at a rate slightly below 60/minute as the cardiac rhythm.
• When looking for occult 2:1 AV conduction (be this from 2:1 AV block — or from atrial flutter with 2:1 AV conduction) — calipers facilitate the process. Simply set your calipers at HALF the R-R interval — and then look in all 12 leads to see if an “extra deflection” can be found at this distance in any of the leads.
• Look especially carefully at lead V1 when searching for extra atrial activity — as it is not uncommon for this to be the only lead in which you clearly see extra atrial activity. 
• If your patient is stable (and you have thee luxury of an extra moment of time) — Consider the use of additional lead systems (ie, a Lewis Lead — See the November 12, 2019 post in Dr. Smith’s ECG Blog).