A 40 yo with Chest pain. Only ECG abnormality is minimal ST depression in I and aVL (computer interpretation: normal)

A former resident sent this.

He asked: "Hey Steve, Wanted to get your thoughts on this EKG:"

What do you think?
The computer called it a normal ECG

Aside: [There is some "sinus arrhythmia", which is indeed a normal finding.  Sinus arrhythmia is sinus rhythm whose rate varies with respiration.  If the longest P-P interval is 120 ms greater than the shortest, it is sinus arrhythmia.  In this case, the longest P-P interval is 1020ms, and the shortest is 740 ms, for a difference of 280 ms.]

Here was my response: "Leads I and aVL bother me (some ST depression), but the rest of it looks totally normal."

He then went on to say: "40-something with chest pain for one hour.  Had episode of nausea and dizziness when it started.  Burning pain subxiphoid and into throat."

Sounds like reflux, right?

But ST depression in I and aVL is abnormal.  It does not usually represent subendocardial ischemia, but rather it is usually reciprocal ST depression, reciprocal to inferior ST elevation.  There is no ST elevation in inferior leads, but it may just be too early to manifest.

So he obtained a second ECG 40 minutes later:

Now there is new STE in inferior leads and much more obvious ST depression in I and aVL.
Still does not meet STEMI criteria, but it is an obvious OMI

And then another one became more obvious:

Cath lab was activated and a 100% RCA occlusion was found.


Learning Points:

1. Beware ST depression in I and aVL.  It may be the first sign of inferior ST elevation.

2. Also beware isolated T-wave inversion in aVL.  This also may be a soft sign of acute inferior MI, before ST elevation.  (But remember that a negative T-wave in aVL is only "inverted" if the QRST angle is wide; in other words, if the QRS is negative, then a negative T-wave has much less significance.  This is also true in lead III.)

How long would you like to wait for your Occlusion MI to show a STEMI? Sometimes serial ECGs minimizes the delay.

Written by Pendell Meyers

An elderly woman presented with acute onset chest pain and shortness of breath. 

EMS showed us their ECG on arrival at her house:

What do you think?

There is sinus rhythm with minimal STE in V1-V3, not meeting STEMI criteria. However, this STE is definitively abnormal in the setting of a normal QRS complex and hyperacute T-wave morphology in V2. There is a small amount of reciprocal STD in V6 with a negative T-wave.

This is subtle but diagnostic for anterior Occlusion MI. V2 never has this appearance in the absence of full thickness ischemia.

We called for emergent cath lab activation.

The cardiologist arrived quickly and was skeptical about these findings on EMS ECG. So while they were trying to explain their interpretation I simply recorded another ECG:

This ended the discussion.

100% mid-LAD occlusion.

LAD now open after intervention.

Peak troponin T was 1.76 ng/mL.



Repeat ECGs after intervention were consistent with successful reperfusion without significant Q-wave development:

Convalescent echo showed EF 41% with anterior, lateral, and apical wall motion abnormalities. 

Given the relatively rapid reperfusion, and the absence of QS-waves, much of the abnormality on echo could be reversible (myocardial stunning, not infarction). 

Learning Points:

Serial ECGs can sometimes turn a difficult decision into a very easy one, but not all OMIs will develop into clear STEMIs quickly, and some OMIs never will manifest STEMI at all. The delay between OMI and STEMI sometimes causes unacceptable loss of myocardium or worse.

Make sure to burn the morphology of lead V2 from the initial ECG into your brain so that you can recognize this pattern in the future.

STE in V1 with STD in V6 in the presence of a normal QRS complex is another piece of evidence consistent with LAD occlusion.

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Comment by KEN GRAUER, MD (4/20/2019):

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With this case — Dr. Meyers addresses a common theme of this ECG Blog = HOW LONG to wait for your OMI ECG to show a STEMI? As we’ve emphasized before, the important “lesson-to-be-learned” — is that there should not be a need to wait! As soon as there is evidence of acute OMI — your cardiology colleague should be called to expedite cath with the goal of acute reperfusion.

• For clarity — I’ve reproduced the first 3 ECGs that were done in this case in Figure-1. In addition to review of why acute OMI is evident from ECG #1 ( = the initial ECG in this case, that was done by EMS on arrival at the patient’s house) — I found serial observation of the lead V2 appearance on these 3 sequential ECGs to be insightful and important to note!

Figure-1: The first 3 ECGs shown in this case (See text).

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WHY ECG #1 is Diagnostic of Acute OMI (Until You Prove Otherwise … )

Dr. Meyers correctly notified the cardiologist-On-Call as soon as he saw ECG #1 because:

• 1) The clinical setting was worrisome ( = an elderly woman with new-onset chest pain).
• 2) Given this history — there is NO way that the ECG appearance of lead V2 in ECG #1 is normal. Relative to the very small QRS amplitude in lead V2 — the ST segment in this lead is disproportionately large, coved in shape (ie,“frowny” configuration) with some ST elevation. This ST-T wave in lead V2 of ECG #1 is clearly hyperacute.

The appearance of other leads in ECG #1 is much less remarkable compared to the appearance of lead V2. The T wave in neighboring leads V1 and V3 looks a bit more-prominent-than-it-should-be given QRS amplitude in these leads — but this change is subtle, and far from diagnostic! (Of the 5 QRS complexes in these leads — some suggest slight ST elevation in leads V1 and V3 — but others don’t). Otherwise, there is no more than nonspecific ST-T wave flattening in the remaining leads. Therefore — Lead V2 is the KEY to the diagnosis in ECG #1. To this, I’d add the following points:

• It is good to be aware that with acute OMI of the 1st (or 2nd) diagonal branch of the LAD — the only chest lead that may show ST elevation is lead V2. There may be a lesser amount of ST elevation in lead aVL, in association with inferior lead reciprocal ST depression — or — early on, the ECG might look similar to what we see in ECG #1.
• Things can change very quickly during the course of an actively evolving acute OMI (See THIS CASE — in which just 8 minutes passed between the 1st and 2nd ECGs). So, early on — acute OMI of the LAD might (and in this case, did) look like ECG #1.
• I suspect one or more of the 3 anterior leads (V1,V2,V3) in ECG #1 are malpositioned. My reason for this suspicion is that I wouldn’t expect the S wave in lead V2 to decrease by as much as it does from neighboring lead V1 — and then, to become deeper at the same time the r wave is becoming taller, as we move from V2-to-V3. In addition, transition of ST-T wave shape from an upsloping ST segment in V1 — to a downward coving ST segment by V2 — and then back again to an upsloping ST segment by V3, is not the pattern of a usual physiologic progression as one moves from V1-to-V3.

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The “Take-Home” Point: As per Dr. Meyers — Use of frequent serial ECGs can be invaluable until the clinical picture is clarified.

• Chest lead malposition is surprisingly common — even when experienced ECG technicians are the ones doing the tracings.
• Given that the cardiologist in this case was skeptical about the diagnosis of acute OMI from ECG #1 — I would have immediately repeated the ECG as soon as I saw this initial tracing because: i) Some form of anterior lead malposition is suggested (See above) — and, immediate repeat ECG after verifying electrode lead placement might have clarified the true status of acute ST-T wave changes; and, ii) Given this patient’s acute symptoms + strong suggestion of hyperacute ECG changes in lead V2 of ECG #1 — there is a definite possibility that you might already see some evolution of ST-T wave changes within the brief time frame between when ECG #1 was done — and when the repeat ECG is completed. NOTE: The reason I’m suggesting to immediately repeat the ECG — is because we are trying to expedite convincing the cardiologist on this case to take this patient to cath as soon as this can be done.
• PEARL #1: There is an easy way to eliminate the possibility of chest electrode lead placement variability when serial tracings are done. Simply mark the spot on the  chest where electrode leads are placed in cases in which lead malposition is suspected. This should guarantee consistency of electrode lead placement for subsequent serial tracings.
• PEARL #2: Be aware that change in the ANGLE of the patient’s bed may alter QRS and ST-T wave appearance in any number of leads. This factor is typically ignored (Have you ever seen notation on an ECG that the patient was too dyspneic to lie flat? — and that as a result, his/her bed was raised to 30 degrees [or to whatever angle the bed has been raised to ... ] at the time the ECG was done).

Comment on Lead V2 Variability in the 3 ECGs in Figure-1:

Dr. Meyers has capably discussed the evolution of serial ECGs done in this case — and then correlated this with cath findings. I wanted to focus on the changing appearance of the QRS complex in lead V2 for ECGs #1, #2 and #3 (Figure-1):

• It is likely that a different technician recorded each of the 3 ECGs in Figure-1 — since more than one ECG machine was used (black vs red grid lines), and the 3 tracings were recorded at different locations (ie, the patient’s house; the ED; and the cath lab). Lead malposition becomes much more likely when a different person is recording repeat tracings.
• I’ve already described why I thought lead malposition is likely for ECG #1.
• Lead malposition is almost certain for ECG #3. One simply would not expect progression from predominant negativity of the QRS in lead V1 — to predominant positivity by lead V2 — to an equiphasic QRS complex by lead V3.
• And yet another QRS morphology is seen in lead V2 of ECG #2 — in which there is a multiphasic, almost null net QRS complex.
• Realizing that this patient has just undergone a PCI procedure — I would not expect the marked variation in lead V2 QRS morphology across these 3 tracings to have been caused by coronary reperfusion. Especially in view of fairly consistent QRS morphology in the lateral chest leads (leads V4, V5 and V6) across these 3 tracings — I think it virtually certain that there has been lead malposition (at least for lead V2) in at least one or two of these 3 tracings.
• BOTTOM Line: As per Dr. Meyers — "Serial ECGs" can sometimes turn a difficult decision (regarding acute cath lab activation or not) into a very easy one. Awareness of how common chest lead malposition is — and, appreciation of when to suspect lead malposition — may prompt earlier repeat ECGs that may help to expedite you being able to convince a reluctant cardiologist of the need for immediate cath.

A Young Man with Sharp Chest pain

Suppose this patient had chest pain.  What would you diagnose?

What is the diagnosis?

OK.  I lied, just so you could assess your reaction to this ECG.

In fact, this patient did NOT have chest pain.  But some day he may show up in an ED with chest wall pain, and he might erroneously be diagnosed with pericarditis.

This is just classic early repol.  This was recorded in an 18 year old otherwise healthy young man who just had a seizure.  There were no chest symptoms at all.  This was his baseline ECG.

Notice:

1. There is diffuse ST elevation, in all myocardial territories.
2. STE is greater in lead II than III
3. There is no reciprocal ST depression, especially none in aVL
4. There is some PR depression, but less than 0.5 mm
5. Spodick's sign is present
6. There are prominent J-waves in almost every lead.

ECGs like this are often attributed to pericarditis, when the vast majority of the time they are simply normal early repolarization.

Here is a great case where such bias led to poor management:

31 Year Old Male with RUQ Pain and a History of Pericarditis. Submitted by a Med Student, with Great Commentary on Bias!

It is true that early repolarization, as defined by J-waves in inferior and lateral leads, is associated with a higher long term risk of ventricular fibrillation.  But it has no bearing on ED management.

Long-Term Outcome Associated with Early Repolarization on Electrocardiography

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Comment by KEN GRAUER, MD (4/19/2019):

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My initial impression on seeing the ECG posted in this case (which I’ve reproduced for clarity in Figure-1) — was that despite the history we were given ( = chest pain) — that the tracing most probably represented Early Repolarization. That said — I was admittedly not 100% certain of this. I’ll explain my thought process by use of 4 words: i) History; ii) Rub; iii) Proportionality; and, iv) Superimposition.

Figure-1: The ECG posted in this case (See text).

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My thought process:

• The HISTORY: There’s a lot to the history when considering acute pericarditis — including age of the patient — clinical likelihood of acute viral pericarditis ( = by far, the most common cause of acute pericarditis in an ED or out-patient center) vs pericarditis secondary to some other underlying disorder — and, the specific nature of the type of chest pain that the patient is having. I’ve summarized some factors to consider in this regard in Figure-2.

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Figure-2: Factors to consider in obtaining the history in a patient who might have acute pericarditis (Excerpted from Grauer K: ECG-2014-ePub).

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• The RUB: During the past 9+ years that I’ve been interpreting too-numerous-to-count ECGs on a daily basis on various internet ECG forums — the overwhelming majority (I’d estimate well over 90%) of ECG cases posted in which acute pericarditis is a diagnostic consideration, fail to even mention cardiac auscultation in listening for detection of a pericardial friction rub. When the pertinent negative of “No rub heard” is not even mentioned in the clinical presentation — it usually means that the clinician did not specifically listen for a rub. While true that acute pericarditis may not necessarily manifest an audible rub at the time you examine the patient — sometimes it does !!! And, IF you are able to hear a definite pericardial friction rub — then you have made a definitive diagnosis within seconds.

Figure-3: Factors to consider regarding physical examination in a patient who might have acute pericarditis (Excerpted from Grauer K: ECG-2014-ePub).

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• PROPORTIONALITY: The numerical amount of ST elevation seen in multiple leads in Figure-1 is impressive (many leads showing ≥3-4mm of ST elevation). That said — when you consider the markedly increased QRS amplitude evident in so many leads (which I have counted and noted in BLUE letters) — proportionally, the relative amount of ST elevation in Figure-1 is not that great. Together with the prominent J-point notching we see in so many leads — the appearance of ST-T waves in this tracing could be perfectly consistent with a repolarization abnormality.
• SUPERIMPOSITION: One factor that I see all-too-often-ignored — is that a patient may start out with an early repolarization picture — and superimposed on this, then develop a case of acute pericarditis. I have NO idea how to rule out this possibility simply by looking at the ECG shown in Figure-1. Finding a prior ECG on the patient may help — but the caveat exists that ST-T wave changes of early repolarization may vary when serial ECGs are obtained. This is why without considering the other factors mentioned above — I would not be 100% certain that the ECG in Figure-1 was simply a repolarization variant. This ECG certainly has many features consistent with a repolarization variant — and acute pericarditis is a far less common entity. But more than just a single ECG is needed when the goal is to be sure that the patient does not have pericarditis.

Tachycardia, fever to 105, and ischemic ST Elevation -- a Bridge too Far

A near 60 year old male called 911 for increasingly severe fever and SOB.  A prehospital ECG was recorded (not shown and not seen by me) which was worrisome for STEMI.

He presented very tachycardic with a very high fever.

Here was his initial ED ECG:

There is sinus tachycardia at a rate of about 140
There is profound ST Elevation across all precordial leads, as well as I and aVL.
QTc was 374, and the formula value was quite high, consistent with LAD occlusion.

A previous ECG from 4 years prior was normal:

This looks like an anterior STEMI, but it is complicated by tachycardia (which can greatly elevate ST segments) and by the presentation which is of fever and sepsis.

If a patient presents with chest pain and a normal heart rate, or with shockable cardiac arrest, then ischemic appearing ST elevation is STEMI until proven otherwise.

But when the clinical presentation is sepsis, one must entertain the possibility that the ST elevation is due to demand ischemia, or some other process, and exacerbated by tachycardia.

It is prudent to treat the other conditions, get the heart rate controlled, and repeat the ECG.

Case continued

A bedside echo was done:

IMG_1678 from Stephen Smith on Vimeo.

Although the quality is suboptimal, it appears to me to show a hyperdynamic heart and possibly and apical wall motion abnormality.

Case Continued

The patient was treated for sepsis and had another ECG 35 minutes later:

Heart rate is still fast at 120
The QTc = 410 ms
There is still scary STE
The formula is still positive

The patient continued to improve and had another ECG at 65 minutes:

QTc = 419
It looks a lot better, though the formula is still marginally positive:
STE at 60 ms after J-point in V3 (STE60V3) = 3.5
R-wave amplitude in V4 (RAV4) = 10
Total QRS amplitude in V2 = 26
Formula value = 18.9
Any value greater than 18.2 should be assumed to be LAD occlusion until proven otherwise.

Tough case.

Cardiology was consulted and they did not think there was an indication for emergent cath lab activation.

He was admitted and serial troponins were measured:

Because of elevated troponins, a next day echo was done:

The estimated left ventricular ejection fraction is 50%.

The estimated pulmonary artery systolic pressure is 37 mmHg + RA pressure.

Normal estimated left ventricular ejection fraction lower limits of normal.

Regional wall motion abnormality-distal septum anterior and apex akinetic

Here is a repeat ECG:

Looks like a reperfused LAD lesion (Wellens' morphology)

The resident asked me what I thought about this case after the fact but before the angiogram.

I said I think there is a fixed stenosis in the LAD and the tachycardia and stress caused a type 2 STEMI.

In this abstract from 2011, we found that 4%(4 of 99) type 2 MI and 38% of type 1 MI had ST Elevation.
https://www.annemergmed.com/article/S0196-0644(11)00829-8/fulltext


An angiogram was done:

It showed no culprit and no coronary disease, but did show a myocardial bridge in the mid LAD.

An excellent review of myocardial bridging, with full text:

https://academic.oup.com/eurheartj/article/26/12/1159/524878

Myocardial bridging is when the coronary artery, usually the LAD, dives into the myocardium.  

Here is an excerpt from the article:

"Normally, only 15% of coronary blood flow occurs during systole, and because myocardial bridging is a systolic event on angiography, its clinical significance and relevance have been questioned. The presence of tachycardia could unmask the ischaemic effect of a myocardial bridge by shortening the diastolic period and increasing the importance of systolic blood flow. Also, tachycardia may worsen ischaemia because of a decrease in diastolic filling time and in coronary flow reserve (a measure of the ability to augment coronary blood flow under stress).  According to one hypothesis, systolic kinking of the blood vessel may cause trauma to the intima and damage to the endothelium, especially at high heart rates. This, in turn, could produce platelet aggregation and vasospasm and result in an acute coronary syndrome."

Summary of the pathophysiology of this case and the ECGs:

This was a type 2 LAD STEMI.  In other words, there was transmural ischemia during the tachycardia due to both demand (high heart rate) and to the effect of myocardial bridging, which would mimic near occlusion.  Then when the heart rate comes down, demand is decreased and full perfusion is restored, just like it is in Wellens’ syndrome.  So the ECG findings are the same as if the patient had an anterior STEMI with reperfusion.  Thus, there is a wall motion abnormality in the distribution of the LAD (not global apical dyskinesis, as in takostubo).  This wall motion abnormality will almost certainly resolved with time (myocardial stunning).

Takotsubo stress cardiomyopathy is also a possibility, but the echo did not have the typical global apical hypokinesis, and the ECG, especially the reperfusion ECG, is more consistent with LAD ischemia.

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Comment by KEN GRAUER, MD (4/15/2019):

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There are 3 aspects about this case that I love: i) It reminds us about the clinically (but not anatomically) uncommon, but very important entity of Myocardial Bridging; ii) It illustrates the concept of a Type 2 MI, with an example in which there was marked diffuse ST segment elevation; and, iii) It illustrates the influence that tachycardia may have on the amount of ST elevation that will be seen.

• Autopsy studies suggest that Myocardial Bridging may be found in as many as 1/3 of adults. But because most cases result in little or no restriction of coronary flow — the condition usually goes unrecognized, unless there is occasion to perform cardiac catheterization. Emergency providers will encounter this condition — so it is good think about it! — CLICK HERE — for my Review on Myocardial Bridging in discussion of another case.
• It is important to remember that not every acute MI with ST elevation is the result of acute coronary occlusion. With a Type 2 MI, despite no acute coronary atherothrombosis — there will be positive Troponin with either new cardiac chest pain — and/or new ischemic ST-T wave ECG changes — and/or new Q waves on ECG — and/or objective demonstration of new wall motion abnormality. The mechanism responsible for Type 2 MIs is oxygen supply & demand imbalance — which may result from a variety of causes including sustained tachycardia, severe bradycardia, coronary spasm, severe anemia, respiratory failure, hypotension/shock — all of which may be exacerbated by significant underlying coronary disease that had been compensated prior to the appearance of the precipitating cause. —  CLICK HERE — for the ESC/ACC/AHA/WHF 2018 Consensus Document on the 4th Universal Definition of MI, in which these concepts are discussed and illustrated.
• Finally — I selected the 1st and 3rd ECGs done in this case to illustrate the difficulty assessing acute ST segment elevation in association with marked tachycardia (Figure-1).

Figure-1: The 1st and 3rd ECGs in this case (See text).

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Discussion of Figure-1: As per Dr. Smith — ECG #1 showed marked sinus tachycardia at ~140/minute — with diffuse ST segment elevation.

• I often find it difficult to determine the precise amount of ST elevation when the heart rate is very fast. For clarity — I’ve added short horizontal RED lines in Figure-1 to show what I took as the “baseline” for assessing the amount of J-point ST elevation for the 2 ECGs in this figure.
• It may be especially difficult when there is marked tachycardia to identify the J-point that defines the number of millimeters of ST elevation. This is because of the tendency for the ST segment to be curved rather than showing a distinct J-point when the heart rate is fast. For clarity — I’ve added BLUE arrows in ECG #1 to show what I took as the J-point in various leads. I accept that others may differ with the location of my arrows. Suffice it to say that there appears to be ≥4-5 mm of ST elevation in leads V2-thru-V5, with a lesser amount of ST elevation in leads I, aVL, V1 and V6.
• Clinical Context is everything! Given the tachycardia + the lack of chest pain in this patient who was thought to have septicemia — I was not convinced that ECG #1 was the result of an acute cardiac event. Tachycardia may sometimes produce a surprising amount of ST elevation — that greatly decreases (or even goes away) when the heart rate slows. As per Dr. Smith — It is prudent to treat the other conditions, get the heart rate controlled — and then repeat the ECG!
• By the time ECG #3 was done — the patient’s condition had significantly improved, and his heart rate had decreased to ~90/minute (Figure-1). Note how at this slower rate — it becomes much easier to make out the change in slope within the ST segment that defines the J-point (PURPLE arrows). It should be clear that the amount of ST elevation is now significantly less.

BOTTOM Line: It’s impossible to be certain how much of an effect the reduction in heart rate between ECG #1 and ECG #3 had in reducing the extent of ST elevation. We simply can’t tell if the degree of flow restriction produced by the myocardial bridge changed during the course of treatment — since many factors may influence to what extent myocardial briding obstructs flow (including disproportionate shortening of the period of diastolic ventricular filling that occurs at faster heart rates). Regardless, comparison of the 2 ECGs in Figure-1 highlights the wisdom of treating other conditions and, then repeating the ECG as the heart rate slows.

• Qualitatively — I thought the straight ST segment take-off in lead V6 of ECG #1 was the most suspicious shape suggesting more than just tachycardia was going on in the initial ECG. And as the heart rate slowed (in ECG #3) — the amount of persistent ST elevation with abnormal ST coving in leads aVL, V6 + the uncharacteristically straight ST segment take-offs in leads V3, V4, V5 all strongly favored an acute ongoing cardiac event. As per discussion above by Dr. Smith — other tests confirmed the diagnosis of myocardial bridging and Type 2 MI.