What if your system adopted the recommendation that a computer "normal" ECG need not be shown to the doctor?

Written by Pendell Meyers with edits by Smith.  Sent by anonymous

A man in his 40s with no previous heart disease presented within 30 minutes of onset of acute chest pain that started while exercising. There was associated shortness of breath and left arm radiation. 

This Triage ECG (ECG #1) was recorded on a chest pain patient at triage at 1906 (top highest quality image, bottom photo including computer algorithm interpretation):

"Sinus rhythm, normal ECG" (This was performed on a Mortara machine, most likely using Veritas algorithm, but I do not have perfect confirmation of that)

This ECG shows an obvious inferior acute coronary occlusion (OMI).  It is clearly missed by the conventional algorithm.  

Many systems now refrain from showing computer "normal" ECGs to the busy emergency physicians at triage because of very poorly conceived articles that say that if the computer algorithm says "normal," the emergency physician should not be bothered.  

Luckily, this institution does show all triage ECGs to the physician, who in this case immediately recognized OMI and activated emergent transfer to the local PCI center.

Here is the ECG interpreted by the Queen of Hearts:

Click here to sign up for Queen of Hearts Access

Here is ECG #2 at 1959 (I believe this is the time of arrival to the PCI center): 

Again, outrageous conventional algorithm interpretation!
Now it is a full blown STEMI of 3 myocardial territories: inferior, posterior, and lateral
But at least it does not call it "Normal."

Queen of Hearts:

The initial troponin (high sensitivity troponin I) returned less than 6 ng/L.  Below the limit of detection.

Angiogram findings included:

95% mid RCA stenosis with occluded distal right PDA secondary to thrombus (peristent OMI). Successful drug-eluting stent placement opening up 95% mid RCA stenosis to 0% residual

Nonobstructive left system disease. 

Left-ventriculogram showed severe infero-apical hypokinesis with LV ejection fraction 50 to 55%. LVEDP 25.   This is a significant loss of myocardium and ejection fraction.  Some function might possibly recover over weeks.

Medical therapy for thrombotic occlusion of distal right PDA.



Formal echocardiogram:

Systolic function is at the lower limits of normal. The ejection fraction is 50% +/- 5% , calculated using biplane MOD. Severe hypokinesis of the mid-apical inferior and inferoseptal myocardium.


Troponin trend:
less than 6 ng/L
933 ng/L

13,386 ng/L, typical of STEMI

(none further measured -- it might have peaked at a much higher level if it had been measured to peak)

Repeat ECGs after PCI:

These are diagnostic of reperfusion.

The patient was discharged home the next day. No further follow up is available.

Learning Points:

You cannot trust conventional algorithms even to find STEMI(+) OMI, even when they say "normal ECG." We have shown many examples of this on this blog.

Queen of Hearts is available and performs well.

Click here to sign up for Queen of Hearts Access

You should not wait for the troponin when the history and ECG is diagnostic. Even in obvious STEMI(+) OMI, the initial troponin can easily be negative in the initial short time from onset of OMI.

The Queen of Hearts diagnoses almost all of these so called "Normal" ECGs with are in fact OMI and she does so with High Confidence:  

See this post of 10 cases:

When the conventional algorithm diagnoses the ECG as COMPLETELY NORMAL, but there is in fact OMI, what does the Queen of Hearts PM Cardio AI app say? (with 10 case examples)

See other relevant posts:

An undergraduate who is an EKG tech sees something. The computer calls it completely normal. How about the physicians?

Three patients with chest pain and “normal” ECGs: which had OMI? Which were normal? And how did the Queen of Hearts perform?

Four patients with chest pain and ‘normal’ ECG: can you trust the computer interpretation?

Chest pain and a computer ‘normal’ ECG. Therefore, there is no need for a physician to look at this ECG.

And literature:

McLaren, Meyers, Smith and Chartier. Emergency department Code STEMI patients with initial electrocardiogram labeled ‘normal’ by computer interpretation: a 7-year retrospective review. Acad Emerg Med 2024;31:296-300

 

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MY Comment, by KEN GRAUER, MD (6/11/2024):

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Recognition of repolarization variants can be challenging. At times, the distinction between a repolarization variant vs the early stage of acute OMI may not be possible solely on the basis of a single ECG.

• To add to this complexity (as per My Comment in the August 22, 2020 post in Dr. Smith's ECG Blog) — the ST-T wave appearance in repolarization variants may be dynamic! On occasion — ST-T wave appearance with repolarization variants may change from one-hour-to-the-next — or, ST-T wave appearance may change due to a difference in heart rate, performance of exercise, or variation in vagal tone — and, sometimes even without any obvious explanation.
• Finally — there is the clinical reality that a patient who has a "baseline" ECG that manifests a repolarization variant — may at some point develop acute coronary occlusion that in part is masked by benign-appearing ECG characteristics of the underlying repolarization variant.
  

 

It is for the above reasons that I was at first uncertain about the ST-T wave appearance in the inferior leads of the initial ECG in today's case (within the light BLUE rectangles in leads II,III,aVF in Figure-1).

• Although the amount of J-point ST elevation in leads II,III,aVF in Figure-1 is more than is usually seen with repolarization variants, and the peak of the T wave in these leads seemed "bulkier" than usual — the upward-concavity shape of the ST segment (ie, "smiley"-configuration) was not unlike that seen in many repolarization variants.
• Small and narrow q waves are seen in each of the inferior leads of ECG #1 — but in this patient with a relatively vertical frontal plane axis, narrow inferior lead q waves are a common normal manifestation of septal depolarization.
• BOTTOM Line: I would not have diagnosed an acute OMI on the sole basis of inferior lead appearance in today's initial tracing.
  

KEY Point: Despite what I felt was the nondiagnostic picture presented by the ST-T wave appearance in leads II,III,aVF — Definitive ECG diagnosis of an acute OMI is present in ECG #1 for the following reasons:

• The clinical history immediately places today's patient in a higher-prevalence group of patients likely to be evolving an acute OMI (ie, a middle-aged man who presents to the ED for new-onset CP [Chest Pain] that occurs during exercise, and lasts for at least 30 minutes!).
• There is no way the ST-T wave appearance in lead aVL can be normal (within the RED rectangle in this lead). True reciprocal ST-T wave depression does not develop with repolarization variants. While some T wave inversion may normally be seen in lead aVL when the QRS is predominantly negative — there should not be J-point depression in such cases (the RED arrow in lead aVL) — and the inverted T wave should not be as "bulky" as it appears to be in lead aVL of ECG #1.
• Once we know in this patient with new CP that the ST-T wave appearance in lead aVL is definitely abnormal (and consistent with reciprocal ST depression) — we then have to presume that the upward-concavity ST elevation in each of the inferior leads is not simply due to a repolarization variant — but instead, must be interpreted as an acute inferior OMI until proven otherwise.
  
•  
• PEARL: Acute posterior involvement is a common accompaniment of acute inferior OMI. Therefore, the fact that the limb leads show an acute inferior OMI — should prompt us to carefully scrutinize anterior leads for any suggestion of posterior involvement.
  
• Having said this — there is no way the ST-T wave appearance in lead V3 of ECG #1 can be normal (within the RED rectangle in this lead). As we often emphasize on Dr. Smith's ECG Blog — there is normally slight, upward sloping ST elevation in leads V2 and V3. The RED arrow in lead V3 highlights the isoelectric (ie, non-elevated) baseline of the J-point in this lead — which in the context of the above ECG findings, strongly suggests acute posterior OMI until proven otherwise.
  
• By the concept of neighboring leads — I strongly suspected that the ST-T wave appearance in lead V2 was also abnormal because: i) There is no more than the most minimal J-point elevation in this lead; and, ii) The T wave appears more pointed than expected (potentially suggesting some posterior reperfusion).
• To EMPHASIZE: I would not perceive lead V2 by itself to be abnormal (especially given how deep the S wave is in this lead) — but because the history and limb lead appearance are diagnostic of acute inferior OMI — and — because lead V3 truly suggests associated acute posterior involvement — I suspected that the subtle changes in lead V2 were probably also abnormal.

Figure-1: I've labeled the initial ECG in today's case — and compare it with the repeat ECG done 53 minutes later.

What Do We Learn from ECG #2?

The diagnosis of acute infero-postero-lateral OMI becomes obvious with the evolution seen in ECG #2: 

• The ST elevation in the inferior leads of ECG #2 has increased — and the shape of this ST elevation has clearly taken on a more acute appearance.
• There is more ST depression in lead aVL — and the shape of this reciprocal ST depression has taken on a "shelf-like" appearance.
• The peaked T wave previously seen in lead V2 has been replaced by ST depression. The upright T wave seen in lead V1 of ECG #1 is also gone.
• There is now frank ST segment straightening, with some definite ST elevation in leads V3-thru-V6.

 

At this point — a STEMI was diagnosed, and cardiac cath with PCI was performed.

• Given the history of new-onset worrisome CP — the initial ECG in today's case was diagnostic of acute infero-postero OMI for the reasons detailed above.
• The fact that the initial troponin was normal does not in any way rule out acute OMI — as the initial troponin is not always elevated.
  
•  
• KEY Point: The comparison between ECG #1 and ECG #2 done just 53 minutes later — shows a dramatic change! Significant ST-T wave abnormalities may evolve over a period of minutes in an actively ongoing OMI. If either the initial ECG in today's case was not recognized as diagnostic of acute OMI — or — the interventionist cardiologist On-Call could not yet be convinced of the need for prompt cath from the initial ECG — it is likely that a repeat ECG done much sooner than 53 minutes later would have satisfied their criteria for cath.
• In cases like this — repeating the ECG every ~10-20 minutes until there are ECG changes sufficient for the patient to be accepted for cath is advised.
  

A man in his early 40s with chest pain a "normal ECG" by computer algorithm. Should we avoid interrupting a physician to interpret his ECG?

Written by Pendell Meyers

A man in his early 40s experienced acute onset chest pain. The chest pain started about 24 hours ago, but there was no detailed information available about whether his pain had come and gone, or what prompted him to be evaluated 24 hours after onset. 

EMS arrived and recorded this ECG:

What do you think?
See same ECG below with computer automated interpretation, using the Glasgow ECG algorithm which apparently is used by many different providers and devices

Amazing that the computer calls this normal. Notice on the right side of the image how the algorithm correctly measures STE sufficient in V1 and V2 to meet STEMI criteria in a man older than age 40.
And yet it still says "normal". 

As most would agree, this ECG shows highly specific findings of anterolateral OMI, even with STEMI criteria in this case. Thus, this is obvious STEMI(+) OMI until proven otherwise.


If the Queen of Hearts AI program had been used instead, this is what the paramedic would have seen:

Many authors advocate that a computer algorithm "normal" or "otherwise normal" reading has such a low rate of important findings that would change management, such that they do not think it is worth interrupting a physician to have the physician overread the ECG. See discussion and links at end of case for more info on this debate.

But the paramedic and the ED physician in this case did not subscribe to this idea. Instead, they reviewed the ECG immediately regardless of the computer interpretation of "normal."

And they of course activated the cath lab immediately, where he was found to have acute thrombotic occlusion (TIMI 0) of the proximal LAD, as well as embolic D1 occlusion. LCX and RCA were described as "normal" in the cath report. LAD and D1 were stented, but flow unfortunately could not be well restored despite efforts (they list the post intervention TIMI flow still as 0). They did mention some faint collaterals from the RCA to the LAD.

After the angiogram, the first high sensitivity troponin I resulted at 7,259 ng/L (99% URL for men is 20 ng/L for this assay). The next four troponins all returned at "greater than 25,000 ng/L", which is simply the lab's upper reporting limit at this institution.

Here is his ECG hours after the interventions:

There is interval improvement, deflation of STE and HATWs, with terminal T wave inversions. Despite the poor flow noted post-PCI on angiogram, the tissue perfusion has improved according to the ECG.

Next day ECG. QS waves in V2 and aVL. Ongoing T wave inversion in V2, I, aVL.

Echo showed hypokinesis of the mid anterior, mid intravascular septum, and apical anterior walls. EF 40%.

Learning Points:

1. You cannot fully trust conventional computer ECG algorithms to find even STEMI(+) OMI, as in this case

2. You can trust them even less to interpret STEMI(-) OMI findings on ECG. 

It is far too premature to say that paramedics and physicians should not be bothered to interpret ECGs labelled as "normal" or "otherwise normal" by the computer algorithm. How many unnecessary interruptions would you accept to find one case like this? by being interrupted???  For me, the number is really, really high. Far higher than what has been studied so far. Perhaps in the future with better automated ECG interpretation, as also seen in this case, it could be different.

Here are 38 cases of "Normal ECG by Computer Algorithm," the vast majority show subtler STEMI (-) OMI on the ECG.

Here are some of them:

A middle aged female with "heartburn" and a "normal ECG" per the computer

Trust a computer read of "Normal ECG" at your peril!

Computer says "normal," troponin undetectable.

This ECG was interpreted as completely NORMAL by the computer: What about it is THE critical finding??

Occlusion/reperfusion through 6 ‘normal’ ECGs

30 yo woman with trapezius pain. HEART Pathway = 0. Computer "Normal" ECG. Reality: ECG is Diagnostic of LAD Occlusion.

65 year old with syncope and a 'normal' ECG: discharge home?

A 50-something with acute chest pain, a computer "Normal" ECG, and a HEART score of 3 (low risk)

30-something woman with a HEART score of zero, EDACS of 2, computer "Normal" ECG, and initial troponin < Limit of Detection

50 year old with acute chest pain, with ‘normal’ ECG and falling troponin

Literature

Emergent cardiac outcomes in patients with normal electrocardiograms in the emergency department. Am J Emerg Med. 2022 Jan;51:384-387. doi: 10.1016/j.ajem.2021.11.023. Epub 2021 Nov 17.

We wrote this editorial on the above paper (full text).  Reference: Bracey A, Meyers HP, Smith SW. Emergency physicians should interpret every triage ECG, including those with a computer interpretation of "normal". Am J Emerg Med. 2022 May;55:180-182. doi: 10.1016/j.ajem.2022.03.022. Epub 2022 Mar 17. PMID: 35361516.

Summary:

This study looked at less than 1000 cases, which is not nearly enough (see below for analysis) and they used cardiologists as the gold standard (a very poor gold standard), NOT presence or absence of Occlusion MI (which we have done in all of our ECG studies, and must be ascertained by 1) TIMI 0/2 flow on angiogram or 2) culprit + TIMI 3 flow and very high troponin. 

So this study is worthless and must be ignored. 

I have here 38 cases of "Computer Normal" ECGs which were critically abnormal and the vast majority are missed acute coronary occlusions (Missed Acute OMI) and most were recognized by the physician.

We wrote this Editorial in the Journal of Electrocardiology in 2019.  Litell JM, Meyers HP, Smith SW. Emergency physicians should be shown all triage ECGs, even those with a computer interpretation of “Normal.” J Electrocardiol [Internet] 2019;54:79–81. Available from: http://dx.doi.org/10.1016/j.jelectrocard.2019.03.003

Excerpt:

"To illustrate the limitations imposed by sample size, recent data from our institution reveal that we identify approximately 225 type I myocardial infarctions (MI) in a typical year. These include about 60 occlusion MI (OMI) with clear ST segment elevation (none of which would be called “Normal” by the computer) and about 165 Non-STEMI. Of the Non-STEMI in our cohort, about 25% will actually have acute coronary occlusion.  While most of these roughly 40 NSTEMI occlusions would be read by the computer algorithm as abnormal in some way (typically nonspecific ST segment or T wave abnormality), they would not be labelled STEMI.  We might conservatively estimate that 5 of these 40 acute OMIs without diagnostic ST segment elevation would be erroneously read by the computer as “Normal.” That is five OMIs per year misread by the computer algorithm as normal. In that same year we collect approximately 24,000 ECGs in our ED, of which 20% are called “Normal” by the computer. Taken together, these data suggest that out of 5000 “Normal” ECGs in a given year, about 5 (0.1%) will actually be acute OMIs that have been misinterpreted by a computer algorithm as completely normal. A sample size of 855 has no chance of generating a meaningful conclusion about the reliability of computer “Normal”.   In fairness, it is not certain that an average emergency physician will catch these few false normals, but they will absolutely go missed if the physician never sees them.We would prefer to be interrupted."

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My Comment by KEN GRAUER, MD (5/23/2023):

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Today's case illustrates a series of important points that we continually emphasize by means of the cases we present on Dr. Smith's ECG Blog:

• Point #1: The paramedics and ED physician in today's case did the right thing by immediate personal review of the initial ECG (and by not accepting the "normal" reading from the computer). Existing computerized ECG interpretation programs are (and have always been) by definition faulty! This is because until recently — computerized programs have been based on STEMI-criteria — which as we have shown, will miss an estimated 25-30% of acute coronary occlusions (See My Comment in the July 31, 2020 post in Dr. Smith's ECG Blog).
• 
  
• Point #2: Today's case illustrates how existing computerized ECG interpretation programs may sometimes miss even STEMI infarctions (!) — as happened in today's case, in which the initial ECG was labeled "normal" by the computer. I have on multiple occasions in this ECG Blog presented my perspective — in that I find existing computerized ECG interpretation programs useful because I know HOW to use them (See My Comment at the bottom of the page in the February 4, 2022 post of Dr. Smith's ECG Blog). But regardless of your opinion of current computerized interpretations — the KEY point is that you should never accept the computer reading as correct until YOU have verified its interpretation with your own eyes! And, if you disagree with what the computer says (because YOU think the ECG suggests an acute process) — YOUR opinion is the one that needs to be followed!
• 
  
• Point #3: Help is on the way! As we have repeatedly shown (evidence today's post — among many others) — the new "Queen of Hearts" (QoH) AI app has demonstrated amazing sensitivity and specificity for recognizing acute coronary occlusions (including both those with or without satisfying STEMI criteria) — so there very soon should be increasingly more widespread use of this superb resource to assist in recognition of acute OMIs (See My Comment at the bottom of the page in the March 31, 2023 post of Dr. Smith's ECG Blog). 
• To Emphasize: As good as the QoH app is for distinguishing between acute OMIs vs non-OMIs — My recommendation will remain for all clinicians to personally review each ECG. That said — clinician accuracy will certainly improve for early recognition of acute OMIs as use of QoH interpretation increases.
• 
  
• Point #4: Once again — the History is a KEY component for optimal ECG interpretation. Specifically, the history in today's case was, "chest pain that started 24 hours earlier — without information about whether the pain came and went, or persisted — nor about what prompted evaluation 24 hours after onset". Awareness of the extended duration of symptoms in today's case (suggesting that symptoms probably were not consistently intense — or we would have expected the patient to present sooner than 24 hours) — prepares us for: i) The established Q wave in lead V2; and, ii) The overall modest amount of ST elevation despite total occlusion on cath of the proximal LAD and 1st Diagonal (See below for further discussion of these findings).
• 
  
• Point #5: The initial ECG in today's case is worthy of a detailed look as to why Dr. Meyers said it shows "highly specific findings of anterolateral OMI". I review these specific ECG findings in Figure-1 — in which I've reproduced and labeled this initial ECG.

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

The Initial ECG in Today's Case:

The rhythm in ECG #1 is sinus at ~65/minute (The rhythm is actually completely regular — with the first 3 beats being repeated in each simultaneously-recorded set of 3 leads). Intervals (PR, QRS, QTc) and the frontal plane axis are normal. There is no chamber enlargement.

• The most concerning lead is lead V2. There is a Q wave in lead V2 that should not be there (RED arrow) — especially since there has been loss of R wave from the small-but-definitely-present initial positive deflection of the QRS complex in lead V1 (ie, BLUE arrow in this lead highlighting the initial r wave in V1). 
• As per computer calculation — there are 2 mm of J-point ST elevation in lead V2, with initial straightening of the ST segment takeoff (GREEN line in this lead). Although some gently upsloping ST elevation is commonly seen as a normal finding in lead V2 — the amount of ST elevation seen in ECG #1 seems excessive, especially in association with the abnormal Q wave, ST segment straightening, and overly wide base of the T wave in this lead. In this patient with 24 hours of chest pain — I interpreted the ST-T wave in lead V2 as hyperacute.
• 
  
• In support that there is hyperacute ST elevation in lead V2 — is the more than 1 mm of ST elevation with surprisingly tall positive T wave in lead V1. In the absence of LVH or bundle branch block — this is rarely a normal finding (especially in a patient with new chest pain and other suspicious ECG findings).
• In addition — there is T wave "imbalance", in that the T wave in lead V1 is taller than the T wave in lead V6 (ie, Comparison of relative T wave amplitude within the dotted RED vs BLUE rectangles in Figure-1).

PEARL: When T waves in each of the chest leads are upright (as they are in ECG #1) — the T wave in lead V1 is usually not taller than the T wave in lead V6. This "imbalance of precordial T waves" is not seen very often — and in the “right” clinical setting, has been associated with acute OMI (See Manno et al: JACC 1:1213, 1983 — and the July 17, 2013 post by Salim Rezaie in ALiEM).

• NOTE: This is not to say that tall, upright T waves in lead V1 might not sometimes be the result of a repolarization variant or a mirror-image reflection of LV “stain” that can sometimes be seen in anterior leads. Instead — it is simply to say that on occasion — I have found recognition of a tall, upright T wave in lead V1 that is clearly taller than the T wave in lead V6 to be a tip-off to an acute coronary syndrome that I might not otherwise have recognized (For more examples of this finding — See My Comments at the bottom of the page in the October 23, 2020 post — in the June 1, 2022 post — and in the March 26, 2022 post of Dr. Smith's Blog).

Additional abnormal ST-T wave findings in ECG #1:

• Neighboring lead V3 is also abnormal. To Emphasize: By itself — I would not necessarily interpret lead V3 as abnormal. But in the context of T wave "imbalance" with strong suggestion of hyperacute ST-T wave elevation in leads V1 and V2 — I interpreted the ST segment straightening (GREEN line) in lead V3 as extension of the acute process.
• P.S.: The fact that a healthy R wave returns in lead V3 — supports our suspicion that loss of r wave (from lead V1-to-V2), and the resultant initial Q wave in lead V2 is "real" and a marker of infarction.
• 
  
• There is ST elevation in lead aVL. As I discussed in My Comment in the November 21, 2020 post in Dr. Smith's ECG Blog — Birnbaum et al (Am Heart J 131:38, 1996) emphasized the diagnostic utility of identifying ST elevation in this lead — with this finding pointing to proximal LAD and/or 1st Diagonal involvement rather than LCx occlusion when there is ST elevation in one or more of the anterior leads. 
• 
  
• Leads III and aVF manifest the mirror-image opposite ST-T wave picture of lead aVL (Comparison of the ST-T waves within the solid and dotted GREEN rectangles in these leads). These are reciprocal changes.
• In the context of mirror-image opposite reciprocal ST depression in leads III and aVF — I interpreted the ST segment flattening in lead II (GREEN line in this lead) as a reciprocal change in this 3rd inferior lead.
• Finally — lead I (the other high-lateral lead) manifests subtle ST elevation with ST segment straightening (GREEN line) — that in the context of other limb lead findings, has supportive implications of the ST-T wave changes in lead aVL.

Putting It All Together:

The initial ECG in Figure-1 is consistent with the history and cardiac catheterization findings of acute proximal LAD (as well as 1st Diagonal) occlusion.

• The proximal LAD location of acute occlusion is suggested by ST elevation beginning as early as in lead V1, with maximal ST elevation in lead V2. This is further supported by ST elevation in lead aVL with reciprocal ST depression in the inferior leads (Inferior lead reciprocal ST depression is much less common when LAD occlusion occurs more distally).
• That said — the overall amount of ST elevation is relatively modest in this initial ECG, which could reflect spontaneous reopening of the "culprit" vessel over the 24 hours when the patient was deciding whether or not to come to the ED.
• Loss of r wave between leads V1-to-V2, with development of an abnormal Q wave in lead V2 on this initial ECG suggests infarction occurred at some point over those previous 24 hours when the patient was still at home. 
• Serial tracings following stent placement confirmed the large extent of myocardial injury. 

A man in his late 40s with chest pain

 Written by Pendell Meyers with edits by Smith

A man in his late 40s with no known medical problems was at work when he suddenly experienced midsternal chest pain radiating down both arms. Approximately 1 hour after onset of symptoms he was triaged at the ED, with ongoing chest pain, normal vitals, and this triage ECG:

What do you think?

Twice, months apart, I sent this ECG to Dr. Smith without any context or other information (I do this many times per day, with many normal or false positive cases mixed in). The first time he responded "acute ischemia but not active occlusion". The second time he responded "LVH and subendocardial ischemia." It is the same response each time: active subendocardial ischemia.

The computer interpretation states "Left ventricular hypertrophy with repolarization abnormality." So it states there is an abnormality, but attributes it to LVH.

There is sinus rhythm with normal QRS (except for borderline high voltage and LAD, some would call it LAFB - LVH can mimic LAFB). There is a tiny but definite hint of STD in V4-V6, maximal in V5 and V6. There is a tiny amount of STD in I and II and aVL. There is a tiny amount of reciprocal STE in aVR. There is a tiny amount of STE in V1. With such a normal QRS complex, none of these ST segment changes are explained by the QRS complex, and all of them must be considered new and significant until proven otherwise. 

In this pattern, with STD maximal in V5-6 with reciprocal STE in aVR, the ECG is diagnostic for supply/demand mismatch ischemia, also known as subendocardial ischemia (as opposed to OMI, or focal subepicardial ischemia). The ECG pattern of supply/demand ischemia is largely identical regardless of the cause, whether or not it is due to decreased oxygen supply (e.g. left main ACS but with collaterals or without total occlusion, triple vessel disease with non-occlusive ACS, decreased blood pressure, hypoxemia, etc.), increased demand (infinite number of non-ACS causes), or both.

Thus, the interpretation of the supply/demand mismatch pattern on ECG depends completely on the clinical context. 

This patient's clinical context is clearly most likely ACS. Therefore the interpretation is acute, active, non-occlusive ischemia until proven otherwise. This could be compatible with left main ACS (but not total occlusion without collateral circulation) or basically any other acute non-occlusive ACS event causing a significant area of supply/demand mismatch. 

So the patient has definite ACS symptoms, with an ECG showing active ongoing ischemia. He should be assumed to have an acute culprit lesion which could fully occlude at any moment, or could cause significant ischemia and complications at any moment even without fully occluding.

Below you can see close-ups of leads V5, V6, and aVR, with and without red lines showing the baseline, highlighting the small but definite and very important STD and STE.

Case Continued:

The ECG was read as sinus rhythm with no signs of STEMI (that's of course true). Due to overcrowding, and thinking that he had normal vital signs and a "normal" ECG, he had initial labs drawn and was sent to the waiting room until a regular room became available. No medicines were given at that point.

Approximately 30 minutes later, he called out for help in the waiting room. He vomited and collapsed, and was found to be in cardiac arrest. CPR was started and he was brought to the resuscitation area where his rhythm was described as "fine VFib." Multiple defibrillation attempts were made, as well as continuous high quality CPR, but there was no change in rhythm, never any brief ROSC. Thrombolytics were considered but not given due to concern that the etiology was not clear, and they stated they were considering aortic dissection as a possible cause. The arrest was called after about 40 minutes.

The troponin drawn at triage resulted at 121 ng/L (upper reference limit 20 ng/L for men). It is unclear whether the team had this information during resuscitation.

An autopsy was later performed, showing no PE or dissection, but an 80% stenosis of the proximal left circumflex artery. The report does not comment on whether there were signs of fresh thrombus at this location, or whether they could tell if there were definitively acute plaque rupture. There was also 50% luminal stenosis of the mid RCA. 

The autopsy report states:

"Myocardial infarcts less than four hours old show no histologic changes so it is difficult to prove an acute myocardial infarct in less than that time period. Correlating the patient's substernal chest pain and coronary artery disease with cardiac arrest and inability to return to sinus rhythm, a myocardial infarct is the presumed cause of death. Pertinent negatives include that there was no evidence of aortic rupture or dissection. There was no pulmonary embolus. There were minimal pathologic changes throughout the body."

We did not need an autopsy to conclude that ACS was the most likely cause of death, but this autopsy obviously supports that theory. It seems overwhelmingly likely to me that the LCX lesion was the acute culprit. It could have caused VF arrest without fully occluding, or it could have fully occluded in the waiting room and then caused VF arrest (without any ECG performed after triage). One third of patients with confirmed STEMI on the ECG do not have 100% occlusion (TIMI 0 flow) at the time of their emergent cath, so it is very likely that a full LCX occlusion could be only 80% at the time of autopsy. But again, one need not have occlusion for ischemia to result in VF arrest.  

Learning Points:

1. Any ischemia can result in ventricular fibrillation, even non-occlusive ischemia.

2. Moreover, non-occlusive thrombi can become occlusive: thrombi are dynamic; they propagate and lyse continuously.   

3. Patients with symptoms that have even just a moderate likelihood of being due to ACS or due to any ongoing ischemia should not be sent to the waiting room.  They need to be on a monitor in case of dysrhythmia, and take priority over most other patients in the ED.

4. Even if you are not certain that ST depression represents ischemia, it is prudent to at least have the patient in a monitored bed while you are undertaking more investigation. These patients should be a "stat placement" to monitored bed.

Commentary

There is confusion created by the educational campaign of "ST elevation in aVR."  Often, the first thought that providers have when they see STE in aVR is that the patient has "left main occlusion," even in a clinical context that is not consistent with ACS.  And yet when this patient with clear clinical ACS presents with1 mm of reciprocal STE in aVR, it was not seen or understood. We have a significant number of unnecessary cath lab activations due to STE in aVR because providers do not understand that it is one of the most common ECG findings in patients who have any significant illness causing supply/demand mismatch. This is why I title my aVR lecture: "Lead aVR: Once "forgotten," now remembered, always misunderstood." It's gotten to the point that cardiology perceives that we are crying wolf. This is one of the most common findings other than obvious STEMI that cardiologists get consulted for, but the majority of the time it is simply supply/demand mismatch due to a variety of etiologies, including AF with RVR, hypovolemia, GI bleed, respiratory failure, sepsis with hypotension, aortic stenosis, and others. 

STD maximal in V5-6 and lead II, with reciprocal STE in aVR, indicates global supply/demand mismatch subendocardial ischemia, which can be due to ACS or non ACS causes.  

It is important to realize that ischemic ST depression due to subendocardial ischemia does not localize to the leads which show ST depression.  There is usually an ST depression vector towards the apex of the heart (leads II and V5, V6), with reciprocal STE in aVR, and if it is very profound, it is often due to left main or LAD ischemia, or due to non-occlusive ACS of any vessel along with disease of all 3 vessels.  However, non-occlusive ischemia of any artery can result in such ischemic ST depression even in the absence of 3 vessel disease.

STD maximal in V1-V4, in contrast to V5-V6, is reciprocal to subepicardial ischemia due to OMI (reciprocal to what would manifest as ST elevation of overlying leads if they were there).   The exceptions are when there is an abnormal QRS to account for secondary STD, such as RBBB or to a non-ischemic etiology of STD such as hypokalemia.  

Stay tuned for our upcoming publication in JAHA on STD maximal in V1-V4 vs. V5-V6.

Aspirin should be given at triage for a clinical history and ECG like this, unless there is some strong suspicion of dissection (not present in this case). Dissection is far less common than ACS.

After a VF arrest, there should be no doubt that this was ACS and that coronory thrombosis was the etiology.  When the patient could not be resuscitated, this patient would have been a prime candidate for ECMO. If he had arrested in cities such as Minneapolis, with refractory VF ECMO programs (before the program was suspended due to Covid), he would likely have been an ideal candidate for ECMO, in a population that seems to be receiving a nearly 50% chance of neurologically intact survival. If ECMO is not an option, and going to the cath lab during arrest is not an option, I would try thrombolytics before ending the resuscitation on a young healthy witnessed ACS arrest.

Transesophageal echo (TEE) can help decide between asystole and fine VF.