Guidelines would (erroneously) say that this patient who was defibrillated and resuscitated does not need emergent angiography

A patient had a cardiac arrest with ventricular fibrillation and was successfully defibrillated.

Here was his initial ED ECG:

Formal interpretation by interventional cardiologist:

There is "Non-diagnostic" ST Elevation in V2-V4 and aVL.  

Therefore, according to ACC/AHA guidelines based on the COACT and TOMAHAWK trials, this patient should not go emergently to angiography.

But there are hyperacute T-waves and this is obviously diagnostic of a proximal LAD occlusion.  It can't be anything else.

Would you enroll this patient in a study that randomizes patients with VF arrest to immediate vs. delayed angiography?

Of course you wouldn't!!  Because the diagnosis is obvious.

The PMCardio Queen of Hearts AI bot knows it is OMI with high confidence:

Click here to sign up for Queen of Hearts Access

The cath lab was activated in spite of the guidelines.

https://www.ahajournals.org/doi/10.1161/CIR.0000000000001194

The COACT trial was fatally flawed (see below).  They did not keep a register of patients who were not enrolled. A patient like this one would not be enrolled because no clinician (ER doc or cardiologist) would enroll such a patient.

A reliable study would keep track of all patients with shockable arrest and analyze the ones who were not enrolled to see their outcomes.  This study failed to do so.  The proof of this is that only 5% of patients enrolled had acute coronary occlusion.  This is FAR LESS than all other studies of shockable arrest.  

First high sensitivity troponin I = 4 ng/L (nearly below the limit of detection)

Angiogram:

--Culprit is 99 % stenosis in the proximal ostial LAD

--LCX is a large OM with a large lateral segment, the lateral segement has a diffuse 90% disease in the ostial proximal segment of it. It will be staged later on this admission.

Echo:

Decreased LV systolic performance with estimated ejection fraction of 35 - 40 %.

Regional wall motion abnormality- mid to distal septum, anterior, anterolateral and apex.

Troponin profile (peaks at 33,672 -- a large MI):

Post PCI ECG:

2 days later:

Summary of the COACT and TOMAHAWK

According to these 2 randomized trials (TOMAHAWK and COACT, references at bottom), there is no utility of emergent angiography for cardiac arrest "without ST Segment elevation."

These studies did not address OMI ECG findings!!!

--There were many problems with the COACT trial.  See my discussion at the bottom.

--And in the more recent TOMAHAWK, most patients were comatose and died of cerebral anoxia.  So if the patient is awake and has ECG OMI findings, there is no reason to believe that angiography should be withheld.

COACT:

The COACT trial was fatally flawed, and because of it, many cardiologists are convinced that if there are no STEMI criteria, the patient does not need to go to the cath lab.

Lemkes JS, Janssens GN, van der Hoeven NW, et al. Coronary Angiography after Cardiac Arrest without ST-Segment Elevation. N Engl J Med [Internet] 2019;Available from: http://dx.doi.org/10.1056/NEJMoa1816897

Should all patients with shockable arrest be taken to angiography regardless of STEMI or No STEMI?

There has long been controversy about whether to take patients with a shockable rhythm without ST Elevation to the cath lab, and a recent randomized trial showed no benefit: Coronary Angiography after Cardiac Arrest without ST-Segment Elevation (COACT).  This study had a fatal flaw: they did not keep track of all the "Non-STEMI patients" who were NOT enrolled, but instead were sent for immediate angiogram.  It was done in Europe, where the guidelines suggest taking all shockable arrests emergently to the cath lab.  So it is highly likely that physicians were very reluctant to enroll patients whom they suspected had Occlusion MI (OMI), even if they did not have STEMI. These physicians did not want a patient with an OMI that was not a STEMI to be randomized to no angiogram.  This strong suspicion is supported by their data: only 22 of 437 (5.0%) patients in this study had OMI.

What percent of shockable arrests without STE have an OMI?  

This large registry in Circulation 2010 reported that at least 1 significant coronary artery lesion was found in 128 (96%) of 134 patients with ST-segment elevation on the ECG performed after the return of spontaneous circulation, and in 176 (58%) of 301 patients without ST-segment elevation. 

5% vs. 58%!!  It is clear that there was signficant enrollment bias in COACT.

We at Hennepin recently published this study

Sharma et al. (with Smith and others) found that among patients with shockable cardiac arrest who had OMI, the initial and subsequent pre-angiogram ECG were only 75% sensitive for OMI, with similar specificity.

Sharma A, Miranda DF, Rodin H, Bart BA, Smith SW, Shroff GR. Do not disregard the initial 12 lead ECG after out-of-hospital cardiac arrest: It predicts angiographic culprit despite metabolic abnormalities. Resuscitation Plus [Internet] 2020;4:100032. Available from: http://www.sciencedirect.com/science/article/pii/S2666520420300321

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MY Comment, by KEN GRAUER, MD (6/29/2024):

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The question of which patients who are successfully resuscitated following cardiac arrest should undergo prompt cath remains under discussion.

• As per Dr. Smith — the intuitive answer should be obvious. IF the initial ECG following successful defibrillation shows evidence of acute OMI — such patients have much to gain from immediate cath with PCI.

For clarity in Figure-1 — I've reproduced the initial ECG in today's case. As per Dr. Smith — the KEY resides with accurate assessment of this tracing.

• The rhythm is ventricular trigeminy (ie, every 3rd beat is a PVC).
• Sinus P waves are clearly seen in lead II. The QRS complex is wide — with QRS morphology most closely related to LBBB (Left Bundle Branch Block) — as determined by the predominantly upright QRS complexes in left-sided leads I and aVL. (Many LBBBs do not develop all positive R waves until more lateral leads than V6 — so the RS configuration in lead V6 here does not rule out LBBB).
• Regardless of whether you classified this conduction defect as "LBBB" vs IVCD (IntraVentricular Conduction Defect) — QRS morphology should be assessed as for LBBB.
• With LBBB — Q waves are not normally seen in leads I and aVL (as the normal left-to-right direction of septal depolarization is reversed as a result of the damaged left bundle branch — which leads to a right-to-left direction for septal depolarization that essentially eliminates "normal" septal q waves). Thus, the Q waves that we see in leads I and aVL of Figure-1 (especially the wide Q in lead aVL) — is indication that septal infarction has occurred at some point in time. As per the bullets below — that "point" in time is most likely the cause of this patient's cardiac arrest.
• 
  
• As per Dr. Smith — the most remarkable ST-T wave findings in ECG #1 — is the ST segment straightening and markedly disproportionate increase in size of the ST-T wave in lead V2 (within the RED rectangle). Despite the conduction defect — there is no way this ST-T wave in lead V2 could possibly be normal. Instead, this obviously hyperacute T wave in lead V2 suggests LAD OMI until proven otherwise.
• 
  
• The next most remarkable ST-T wave findings are seen within the BLUE rectangles (ie, within Leads I and aVL). Normally — the ST-T waves with simple RBBB or LBBB are oppositely directed to the last deflection of the QRS in these left-sided leads (For more on these findings with LBBB — Please check out My Comment in the September 17, 2020 post in Dr. Smith's ECG Blog).
• Instead, in lead I — the ST segment is not in the least depressed, and the T wave is upright in this lead (whereas in lead I — there should normally be ST-T wave depression). This is a primary ST-T wave change, that in a patient with chest pain (or cardiac arrest) — indicates an ongoing acute event until proven otherwise.
• Even more remarkable — is the ST segment coving with hint of ST elevation and T wave inversion in lead aVL. This shape of ST-T wave in lead aVL is the opposite of the ST-T wave depression expected in lead aVL when there is LBBB. Simply stated — the shape of the ST-T wave in lead aVL looks like an evolving acute MI (and further supports indication of acute LAD occlusion).
• 
  
• In SUMMARY: In a patient who has just been defibrillated following cardiac arrest — it is hard to imagine how ECG #1 could be interpreted in any way other than representing acute LAD OMI in need of prompt cath with PCI. 

Figure-1: I've labeled the initial ECG in today's case (recorded after successful defibrillation).

 

A woman in her 50s with multiple episodes of syncope

By Sofiya Diurba MD, reviewed by Meyers, Grauer

A woman in her 50s with PMH known RBBB and prior syncopal events presents to the ED for five syncopal events over the last 24 hours. Each event is associated with a prodrome of mild substernal CP, SOB, and “brain fog.” EMS reports intermittent sinus tachycardia and bradycardia secondary to some type of heart block during transport. They note that the patient consistently became more symptomatic when bradycardic but had no hypotension.

Smith comment: Go here for a comprehensive blog post on syncope and link to the most detailed version of the Canadian Syncope Rule: Emergency Department Syncope Workup.  

She remained normotensive but experienced fluctuations in her symptoms of feeling “like I am about to pass out." Vital signs were within normal limits at the time of triage.


This is her first ECG in the ED:

What do you see?

This ECG shows both a right bundle branch block and a posterior fascicular block. It is hard to make out P waves but you can see them best in V2, and notches in the T waves in other leads - this is a sinus tachycardia with a very long PR interval indicating first degree block.

Smith comment: Bifascicular block with first degree AV block is called "Trifascicular Block."  Although it is somewhat of a misnomer, it portends high grade AV block.  See these blog posts.

But please see Ken Grauer's in depth and fascinating analysis at the bottom of the post if you want to learn why it is actually more complicated than just simple sinus rhythm!



Another ECG is taken about twenty minutes later and shows this:

The rhythm is complex and variable, but overall shows various degrees of AV block. QRS complexes have similar RBBB morphology to the prior ECG. By the end of the ECG, there is 1:1 conduction. 

See Ken Grauer's detailed diagram explaining each beat, at the end of the post.  He shows how this ECG manifests Dual AV nodal pathways.

The providers were appropriately concerned for symptomatic high grade AV block.  They knew she would need a pacemaker unless some transient and reversible cause was discovered. 


Labs including electrolytes, CBC, troponin, BNP, TSH, and LFTs were largely unremarkable without any explanation for the ECG findings.


Cardiology was consulted and the patient had a few more ECGs recorded while in the ED that show even higher grade, more severe, 2nd degree AV block. 

While awaiting admission to cardiology service, the patient had the following rhythm for approximately ten seconds on the monitor (representative image, courtesy of “ECG Educator Blog”):

The patient is in ventricular standstill with no conducted P-waves and no underlying junctional or ventricular escape rhythm kicking in. She briefly became unconscious during this episode but went back into a second/third degree alternating rhythm and did not require chest compressions. Pads were immediately placed to transcutaneously pace. Once this happens, of course, the patient will require temporary or permanent pacemaker as soon as possible.

With ongoing transcutaneous pacing, Cardiology emergently took the patient to the cath lab for temporary pacing wire placement via right IJ which she tolerated well.


She required intermittent pacing from the temp wire numerous times overnight so a permanent  pacemaker was placed the next day. The echocardiogram showed a normal EF without any abnormalities. Troponins were all negative. There was no apparent reversible cause found for the worsening heart block. She was discharged with plan for outpatient cardiac MRI for further evalution.



Here is her ECG prior to discharge:

This shows a ventricularly paced rhythm. Her heart block was successfully treated!




Learning Points:


When patients have a bifascicular block, they only have one tiny little fascicle holding on to conduct a signal from the atria down to the ventricles. When a patient with bifascicular block presents with intermittent second or third degree heart block, they need urgent or as in this case, emergent, intervention to prevent a persistent complete heart block or asystole as this patient experienced.

Don’t forget the WOBBLER pneumonic for what to look for on an ECG for dangerous cardiac causes of syncope in a patient who presents with syncope (courtesy of Dr. Smith’s ECG blog):

WPW

Obstructed AV pathway (meaning AV blocks)

Brugada

Bifascicular block

LVH (including HOCM and other entities with LVH such as aortic stenosis)

Epsilon wave (ARVC)

Repolarization (both short and long QT)

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MY Comment, by KEN GRAUER, MD (6/27/2024):

===================================

As one who loves the challenge of interpreting complex arrhythmias — I could not resist the urge to "dive into" the fascinating conduction blocks in today's tracing. While fully acknowledging that I am not certain about my proposed mechanism for all that we see — my hope is that the concepts I suggest prove insightful.

• To EMPHASIZE: What follows are advanced concepts that extend well beyond what is needed for appropriate emergency management of today's patient. Limiting one's interpretation to marked bradycardia with high-grade AV block in need of pacing in this patient with multiple syncopal epiosodes — more than suffices for "the quick answer". But for those with an interest in going further — I'll add the following considerations.

===========================================

General Concepts:

• I do not see evidence of intermittent complete ( = 3rd degree) AV block. The easiest way to quickly recognize complete AV block — is to remember that most of the time, the escape rhythm will be regular (or at least fairly regular) when there is complete AV block — and this is not the case in today's series of rhythms.
• Further evidence against there being complete AV block — is the presence of a definite "pattern" to these rhythms, with 2 PR intervals that continually repeat. Identifying PR intervals that repeat means that there is at least some conduction (therefore ruling out complete AV block).

The Initial ECG (which I've labeled in Figure-1):

For clarity in Figure-1 — I've labeled the initial ECG in today's case. As per Drs. Diurba and Meyers — this initial ECG reveals a rapid supraventricular rhythm with RBBB/LPHB (ie, all postive QRS in V1 with wide terminal S waves in lateral leads I and V6 — with predominant negativity for the straight portion of the S wave in lead I indicative of associated LPHB).

• The rhythm is not simple sinus tachycardia. Although P waves are fairly regular (ie, the arrows I've added in lead II corresponding to the notches highlighted by Drs. Diurba and Meyers in lead V2) — the ventricular rhythm is not regular.
• Instead of a regular ventricular rhythm — there is a bigeminal pattern with a slightly longer R-R interval (dark BLUE bars) that alternates with a shorter R-R interval (light BLUE bars). This is subtle! — but caliper measurement confirms this consistent pattern.
• Careful observation (best seen in the long lead II rhythm strip of Figure-1) — also confirms a consistent change in T wave morphology that occurs every-other-beat. This is real — and not due to chance. Caliper measurment confirms that the PR interval alternates from a slightly longer PR interval (RED arrow P waves) — to a PR interval that is shorter (PINK arrow P waves).

These observations had me stumped ...

• The only plausible explanation I could come up with for why the atrial rate (P-P interval) would be constant — but the PR interval was alternating from a longer-to-shorter interval without ever dropping a beat — would be if the patient had dual AV nodal pathways, and was switching from one-to-the-other pathway every-other-beat. 

Figure-1: I've labeled the initial ECG in today's case.

Figure-2: In Support of My Theory ...

As per Drs. Diurba and Meyers — there is LOTS going on in Figure-2.

• The atrial rhythm (P-P interval) remains constant, still at a rate over 100/minute (colored arrows in Figure-2).
• Beat #2 is a fusion beat (the on-time BLUE arrow P wave does not have enough time to conduct to the ventricles — so it fuses with a ventricular escape beat that arises because of the overly long preceding R-R interval).
• 
  
• I suspect there is LA-RA Lead Reversal (See My Comment in the August 17, 2022 post of Dr. Smith's ECG Blog for review of the effects of LA-RA reversal). Although hard to prove lead reversal after-the-fact, especially given bradycardia and the fusion beat — but supraventricular beats #2 and 3 suddenly look like lead aVR looked — and lead aVR suddenly looks like lead I looked like in Figure-1 when we saw the LPHB. 

The "good news" (from an arrhythmia interpretation perspective) — is that we now see P waves much better than we did in the initial ECG. 

• ECG #2 begins with what appears to be high-grade 2nd-degree AV block (ie, We see 2 non-conducted YELLOW arrow P waves in a row prior to beat #1).
• There follows 2 consecutively conducted P waves with the same slightly longer PR interval that we saw in Figure-1 (RED arrow P waves before beats #2 and 3).
• This is followed by a number of cycles of 2nd-degree AV block with 2:1 AV conduction (RED arrow P waves in front of beats #4,5,6,7,8 all with the same longer PR interval that we saw in Figure-1 — and YELLOW arrow P waves being the dropped beats.).
• Figure-2 ends with 4 beats of 1:1 conduction — but this time, we see the slightly shorter PR interval (PINK arrows preceding beats #9,10,11,12).
• 
  
• NOTE: The fact that the PR interval of all RED arrow P waves in Figure-2 remains the same, confirms definite conduction (ie, There is no evidence of complete AV block). The same is true for the similar, slighty shorter PR intervals for each of the 4 PINK arrow P waves at the end of the tracing — with my theory as the reason for alternating PR intervals of conducted beats being that there are dual AV nodal pathways, with each manifesting AV block!

Figure-2: I've labeled ECG #2.

Figure-3: More Severe AV Block ...

I've continued my color coding of P waves in ECG #3.

• NOTE: I suspect there once again is LA-RA lead reversal in Figure-3.
• 
  
• We see more evidence of higher-grade 2nd-degree AV block in Figure-3 — as we see 2 and 3 consecutive P waves that are not conducted (YELLOW arrows representing on-time P waves that are blocked). That said — we know that ECG #3 is not complete AV block, because the PR interval of all RED arrow P waves remains constant (and remains the same PR interval as for RED arrow P waves in Figures-1 and -2 discussed above).
• Once again — PINK arrow P waves represent conducted beats with the same slightly shorter PR interval as was seen in Figures-1 and -2.
• NOTE: Even accounting for the fact that part of these PINK arrow P waves are "cut off" by the preceding T wave — caliper measurement confirms that the PR interval of these PINK arrow P waves is shorter than that of the RED arrow P waves. These are not PACs — because these PINK arrow P waves occur precisely on time! And the only way I know to explain how the PR interval of on-time P waves would shorten without ever dropping a beat — is if there are dual AV nodal pathways, each with their own degree of high-grade 2nd-degree AV block.

Figure-3: I've labeled ECG #3. 

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BOTTOM Line in Today's CASE = The patient needed a pacemaker!

• That said, for readers with an interest in complex arrhythmias — Isn't this series of serial tracings fascinating!

===========================================

OMI can be very subtle and easy to miss, but be a very large infarction.

I was reading ECGs on the system and came across this one.  

What do you think?

There is minimal STE in II, III, with an inverted T-wave in aVL.

There is a very flat ST segment in V2, with 0.5 mm of STD, highly suspicious for posterior OMI.

We showed in this paper that ANY amount of STD maximal in V1-V4 (especially in V2) in a patient with chest symptoms is posterior OMI until proven otherwise

I knew that if this is a patient with chest discomfort, that it is an infero-posterior OMI.

So I went to the chart and found that it was from a 50-something woman with CP of a couple hours duration.

Unfortunately, the OMI was not seen.

The Queen of Hearts AI bot also sees "OMI with High Confidence."

Click here to sign up for Queen of Hearts Access

Case Continued

When the first troponin returned slightly elevated, this ECG was recorded 100 minutes later (too long to wait for a repeat ECG!!):

Now it is not subtle: there is clear, obvious inferior posterior OMI.

At this point, the cath lab was activated.  Angiography showed:

100% Distal RCA occlusion. Pre-procedure TIMI 0 flow was noted. Stent placed.  Post Procedure TIMI III flow was present. 

ECG recorded after PCI:

Large upright T-waves in V2, V3 indicated posterior reperfusion.

Later after PCI:

Trop went over 50,000 ng/L very quickly.  This is a very large MI. 

Such a large amount if infarction could have been avoided with earlier OMI recognition!!

Echo:

The estimated left ventricular ejection fraction is 58 %.

Regional wall motion abnormality basal-inferior (this is the posterior wall), akinetic.

Regional wall motion abnormality basal inferoseptum, akinetic.

Learning Points:

1. Acute 100% coronary occlusion can be VERY subtle on the ECG.

2. Use the Queen of Hearts AI to make the diagnosis quickly!

3. Record serial ECGs every 15 minutes!!  Even if you don't see the OMI, you can usually prevent such a long delay to reperfusion by recording serial ECGs every 15 minutes for a patient with persistent chest pain.  Hillinger et al. showed that ST Elevation criteria are 21% sensitive for OMI on the first ECG, and 30% sensitive on serial ECGs.  

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My Comment by KEN GRAUER, MD (6/25/2024):

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For many reasons — I thought today's post by Dr. Smith to be highly insightful and extremely useful to any provider charged with interpreting emergency ECGs. These reasons include:

• Recognition of the importance of having someone "overread" ECGs in the clinical setting in which you work.
• The initial tracing in today's case — serves as an excellent test to see how good YOU are at recognizing a subtle OMI that should not be missed!
• The serial tracings in today's case provide a superb review of the ECG evolution of an acute OMI with subsequent reperfusion.
• Finally — today's case provides a challenge to see IF you recognize some subtle-but-important lead placement issues that appear on serial tracings?

Having Someone "Overread" ECGs in Your Clinical Setting:

Today's case arose by chance — as Dr. Smith was simply reading ECGs posted on his hospital system (without the benefit of any clinical history).

• I performed this function for 30 years in our primary care residency clinic — where I overread all tracings for our 35 medical providers. My experience was similar to that described in today's post — in that I would often see things on an ECG which I thought might not have been noticed by the provider(s) caring for the patient. This would lead me to pull the chart and/or directly call the medical care provider to find out happened clinically.
• This experience served as a "quality control" — in that I learned to appreciate the ECG interpretation skills of our providers. It would also pick up a small but important percentage of cases in which an important ECG finding potentially having a direct impact on patient care would have been missed had I not been overreading ECGs. 
• 
  
• QUESTION: Is there an expert interpreter overreading the ECGs in the clinical setting where YOU practice? If not — Do you think this would be helpful? In today's case — it enabled providing feedback to the clinician who missed the subtle-but-important ECG signs of acute OMI.

Although Subtle — this OMI Should Be Recognized!

I agree with Dr. Smith — that the acute OMI evident on today's initial tracing is subtle. That said, in my opinion — the experienced emergency care provider should within seconds — recognize that if ECG #1 (that I have reproduced in Figure-1) is obtained from a patient with new chest pain — that this tracing is diagnostic of acute OMI until proven otherwise!

• The rhythm in ECG #1 is sinus bradycardia and arrhythmia. The lead that immediately caught my eye —  is lead aVL. Although the T wave in lead aVL will often normally be negative when the QRS in this lead is predominantly negative — the inverted T wave (at least for the 1st QRS complex in this lead) — is disproportionately hypervoluminous.
• Support that this abnormal ST-T wave finding in lead aVL is "real" — is forthcoming from the abnormal appearance of the abnormally straightened ST segment in lead I.
• NOTE: I fully acknowledge that there are baseline artifactual undulations in the limb leads of ECG #1 — and that there is beat-to-beat variation in QRST appearance, raising the question as to which beat is the "real" one. That said — the ST segment straightening in lead I is seen in all 3 of the QRS complexes present in this lead. This confirms that this ST segment straightening is a real change — and it supports our concern about the hypervoluminously inverted T wave in lead aVL.
• 
  
• In lead III of ECG #1 — the ST-T wave is not normal. While fully aware that the ST-T wave appearance for each of the 3 beats in lead III varies — there does appear to be straightening of the ST segment takeoff, with at least a slight amount of abnormal ST elevation. In association with the reciprocal changes suggested in high-lateral leads I and aVL — this should raise concern for acute inferior OMI.

Confirmation that the above subtle limb lead changes are real — is forthcoming from the definitely abnormal ST-T waves in leads V2-thru-V6. 

• As we have often emphasized regarding the normal appearance of the ST-T wave in lead V2 and lead V3 — there is normally slight ST elevation, with a gradually upsloping shape of the ST segment, as it imperceptively blends into a normally upright T wave.
• Instead — the ST segment in leads V2 and V3 of ECG #1 is unmistakably flat, if not slightly depressed. As per Dr. Smith — this abnormal ST segment appearance in these anterior suggests posterior OMI — especially in association with the limb lead changes just described that suggest inferior OMI.
• Abnormal ST segment straightening continues in leads V4,V5,V6 of ECG #1. While fully aware of the difficulty of knowing which of the 2 QRST complexes in these lateral chest leads is the "real" one — there is at the least, abnormal ST flattening with slight ST depression.
• 
  
• PEARL #1: Dr. Smith instantly recognized that if ECG #1 was from a patient with new chest pain — that this tracing represents acute ongoing infero-postero OMI until proven otherwise. The words that I use to describe the abnormal ST-T wave findings do not do justice to this ECG diagnosis. Instead — it is the "picture" of the hypervoluminously inverted T wave in lead aVL — in association with the straight takeoff and ST elevation in lead III — in association with the "shape" of the ST flattening and depression in multiple anterior leads — that tells the experienced interpreter within seconds that there is acute infero-postero OMI.
• 
  
• PEARL #2: When asking myself IF the ST-T wave changes I am contemplating are "real" — I look first for those 1, 2 or 3 leads that I know show abnormal changes. In a patient with new chest pain — there is no way that the inverted T wave in lead aVL and the ST flattening with slight depression in anterior leads is "normal". Once I've identified a few definitely abnormal leads — it becomes easier to recognize less marked ST-T wave abnormalities in neighboring leads.
• 
  
• PEARL #3: Because the acute OMI was not recognized in ECG #1 of today's case — a 2nd ECG was not done for well over an hour. As per Dr. Smith — by the time ECG #2 was recorded (ie, 1:37 after ECG #1) — the diagnosis of acute infero-postero OMI had become obvious. 
• KEY Point: Even if one was uncertain about an acute OMI from assessment of ECG #1 — at the very least, the abnormal ST segment flattening in multiple leads of this initial tracing should have been recognized. 
• IF ever in doubt about whether an acute event may be ongoing — Repeat the ECG within 10-to-15 minutes (since dynamic ST-T wave changes during an actively evolving event may occur with surprising rapidity). 

 

Figure-1: The first 3 ECGs in today's case.

The Evolution of ECG Changes with Acute OMI:

It's instructive to review the serial tracings recorded during the evolution of an acute OMI. Doing so is a great way to hone skills for recognizing subtle findings on the initial tracing — that rapidly evolve into "tell-tale" abnormalities.

• Note that what seemed to be very subtle ST-T wave changes in lead aVL and lead III in ECG #1 — has blossomed into obvious abnormalities in ECG #2. The volume of the inverted T wave in lead aVL has deepened — and — the ST segment takeoff straightening with J-point ST elevation has clearly accentuated in the repeat ECG.
• The evolution of serial ECG changes between ECG #1 and ECG #2 — is even more marked in the chest leads. Increased J-point ST depression, with downslope sagging ST segments and terminal T wave positivity (ie, markedly positive "Mirror" Test — as per My Comment in the September 21, 2022 post of Dr. Smith's ECG Blog)  — confirms acute posterior OMI.
• 
  
• As per Dr. Smith — cardiac cath revealed 100% distal RCA occlusion. ECG #3 (performed just after successful PCI) — provides the classic picture of posterior wall reperfusion T waves in leads V1-thru-V5 (ie, resolution of the ST depression seen in ECG #2 — with evolution to tall, now completely positive T waves).

Subtle-but-Important Lead Placement Issues:

In Figure-2 — there are 2 subtle-but-important lead placement issues evident over the course of the 3 serial tracings in this figure. Can YOU identify them?

Figure-2: Comparison of the 2nd, 3rd and 4th tracings in today's case. Can you identify the subtle-but-important lead placement issues raised over the course of these serial tracings?

ANSWER:

Its essential when comparing serial tracings to make sure that technical aspects of the ECG recording remain constant. By this I mean — that the frontal plane axis does not significantly shift from one tracing to the next — and that precordial electrode lead placement does not significantly vary. Even change in the angle of the patient's bed may affect QRST appearance in a number of leads.

• Did YOU notice that there has been a marked leftward shift of the frontal plane axis in ECG #3? By chance — Did you also notice that the P wave in lead I of ECG #3 is now larger than the P wave in lead II?
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• Did YOU notice that leads V1 and V2 of ECG #4 were placed too high on the chest?

LA-LL Lead Reversal:

We periodically show cases with technical mishaps that often go unnoticed (Please see My Comment at the bottom of the page of the August 17, 2022 post in Dr. Smith's ECG Blog for a series of links with illustrative cases).

• The reason for the surprising marked shift in frontal plane axis seen in ECG #3 of Figure-2 — is that there is LA-LL Lead Reversal! This is relevant — because QRST morphology in the limb leads of this tracing obtained shortly after PCI is otherwise confusing!
• I review in detail the approach to recognizing LA-LL Lead Reversal in My Comment in the May 26, 2022 post of Dr. Smith's ECG Blog. PEARL #4: In addition to the unexplained marked frontal plane axis shift — the "tipoff" to LA-LL Reversal — is that the P wave in lead I of ECG #3 is clearly larger than the P wave in lead II (and this is distinctly unusual when there is sinus rhythm).
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• In Figure-3 — I account for correction of the changes produced by LA-LL Lead Reversal. Note in ECG #3a — that the frontal plane axis and QRS morphology in each of the limb leads now looks very similar (as it should be) to QRS morphology in the limb leads of ECGs #1, 2, and 4. Note also in ECG #3a — that the P wave in lead II is once again clearly larger than the P wave in lead I (as it should be with sinus rhythm).
• Finally, in ECG #3a — Note the presence of the expected ST-T wave reperfusion waves in the limb leads for this patient with infero-postero OMI (ie, T waves now positive in lateral leads I and aVL — and T wave inversion in lead III).

Figure-3: Comparison of ECG #3 before and after correction for LA-LL Lead Reversal.

Too High Lead V1,V2 Placement in ECG #4:

Last but not least — it's clinically important to recognize that leads V1 and V2 in ECG #4 (from Figure-2) were placed too high on the chest. As I review in detail My Comment in the April 17, 2022 post in Dr. Smith's ECG Blog — the ECG findings that define this lead placement error are:

• Clue #1: There is an rSr' in leads V1 and V2, in the absence of incomplete RBBB (ie, no terminal s wave in lateral leads I and V6).
• Clue #2: There is a deep, negative component to the P wave in leads V1 and V2.
• Clue #3: The appearance of the QRS complex and the ST-T wave in leads V1 and V2 very much resembles the appearance in lead aVR.
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• NOTE: The clinical relevance of immediately recognizing too high placement of leads V1,V2 — is that we lose the evolutionary reperfusion T wave findings that we were expecting to see in this post-PCI tracing.