Patient with Dyspnea. You are handed a triage ECG interpreted as "normal" by the computer.

I was handed this ECG of a patient with dyspnea:

What do you think?

Computer interpretation: Normal EKG
Physician Overread (Final interpretation): Normal EKG

The ST segment is very flat, with a sudden rise to the peak of the T-wave.  This makes the base of the T-wave look very narrow.  A narrow-based T-wave is nearly pathognomonic for hyperkalemia.  My diagnosis was hyperkalemia.

The resident I showed it to saw nothing.  I explained all this to the resident, then went to see the patient.

Turns out he is a dialysis patient.

Later, the ECG computer interpretation was overread by another physician, and that physician thought it was normal, but took the step to compare with the most recent previous ECG.  There was no change, so that physician concluded that it was indeed normal and entered "Normal EKG" as the final diagnosis.

However, I looked a bit more in depth, and the previous ECG had also been recorded during hyperkalemia.

The K returned at 6.3 mEq/L.

Let's look at a couple previous ones from 2 years prior:

This was recorded when this patient presented with diaphoresis and muscle cramps:

The formal read was normal except for "possible old lateral MI"
QTc was measured at 484 ms which appears to be accurate, but the statement did not say "long QT"

There are definitely peaked T waves, and a long flat ST segment with an abrupt rise to the peak of the T-waves.

The K was 6.6 mEq/L

What else do you suspect?

This ECG was recorded a few hours later after bringing down the K to 4.8 mEq/L.:

These are now normal T-waves.
Can you see the difference between these and the T-waves in the 1st 2 ECGs?

Computer interpretation AND physician overread:
Normal except for long QT (486 ms)

The other thing you might have suspected is hypocalcemia, as the long QT is long because of a long ST segment (not because of a wide T-wave). 
The (not ionized) Ca on these 2 ECGs was 6.4 mg/dL (very low)
On the first ECG above, the QTc was 402 ms and the Calcium was normal.

The diagnosis was fluid overload and hyperkalemia.  Dialysis fixed both.

Learning Points:

1. Peaking of T-waves can be very subtle
2. Comparison with previous must be done with a previous that is recorded in the presence of a normal K.
3.  Peaked Ts are not necessarily large or tall.  They have a narrow base, and a sharp upstroke.  Often they look as though they would puncture you if you sat on them.
4.  Early repolarization and even LVH can have T-waves that mimic hyperK.
5. Having the physician read every EKG, whether the computer calls it normal or not, is of course only useful if the physician can recognize the abnormality

If you miss hyperK T-waves, your patient may have an unexpected cardiac arrest:

Here is a really interesting post, in which a patient with very subtly peaked T-waves, which are misinterpreted as early repolarization, has a ventricular fibrillation arrest before the K returns high:

HyperKalemia with Cardiac Arrest. 

Peaked T waves: Hyperacute (STEMI) vs. Early Repolarizaton vs. Hyperkalemia

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Comment by KEN GRAUER, MD (6/15/2019):

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Instructive case! I focus My Comments on ECG #1 = the initial ECG obtained in the ED (Figure-1). In my opinion, rather than calling this ECG “normal” (as did 2 clinicians and the computer) — there are 4 ECG findings that should be noted: i) Prolonged QTc; ii) LVH, clearly by voltage; iii) ST segment straightening in multiple leads; and, iv) Tall, peaked (and pointed) T waves with a narrow base in at least 4 of the 6 chest leads. 

• While I fully acknowledge that some of these ECG findings are subtle — I submit that recognition that this ECG is not “normal” would not have been overlooked IF interpreters had used a Systematic Approach (For “My Take” on how routine use of a Systematic Approach not only improves accuracy, but also speeds you up — See Dr. Smith’s May 7, 2019 Blog).

Figure-1: The initial ECG done in the ED (See text).

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

Beginning with Descriptive Analysis:

• There is baseline artifact in ECG #1 — which is most marked in the limb leads. That said, this does not prevent accurate interpretation of the key findings.
• Rate & Rhythm — The rhythm is sinus at ~85/minute. Intervals — The PR interval is normal. The QRS complex is not wide. However, the QTc is somewhat prolonged. I measure the QT = 400 msec (See markings in lead V3). Correcting for the heart rate of 85/minute — I estimate a QTc ~470-480 msec (which is clearly above the upper expected range ~440 msec).
• Axis — The frontal plane QRS axis is normal (about +30 degrees).
• Chamber Enlargement — There is no atrial abnormality, and no RVH. But voltage criteria for LVH are definitely satisfied! I have reviewed “My Take” on a user-friendly approach to ECG diagnosis of LVH in Dr. Smith’s April 27, 2019 Blog. For ease of recall — I’ve excerpted the user-friendly criteria I favor in Figure-2. ECG #1 is an example in which the most commonly helpful criteria (35 & 12 — as per Figure-2) are negative — but both Cornell Criteria (R in aVL + S in V3 ≥28 for a man) and especially Peguero Criteria (deepest S + S in V4 ≥28mm for a man) are met. NOTE: Short, horizontal BLUE lines in leads V4 and V5 indicate the limits for R wave and S wave amplitude in these leads, in which overlap of complexes makes assessment a bit challenging.
• Q-R-S-T Changes — There are small, narrow Q waves in leads V5 and V6 (most probably normal septal q waves). R Wave Progression — shows slightly delayed transition (the R becomes taller than the S wave is deep between lead V4-to-V5). ST-T Waves — show ST segment straightening (short PURPLE lines in leads V4,V5,V6) and frank ST flattening (PURPLE lines) in leads V2 and V3. This is not normal — as the ST segment should normally be gently upsloping (Please see My Comment in Dr. Smith’s June 9, 2019 Blog). And, there is even a hint of ST depression in leads V5 and V6.
• As noted by Dr. Smith — it is because of this ST segment straightening and flattening in multiple chest leads — that the abnormal shape of the T waves in leads V2-thru-V6 should be noted. As a memory aid — the shape of the Eiffel Tower (= tall and rising to a point at the top, but with a surprisingly narrow base) — should recall the shape of typical hyerkalemic T waves (See Figure-1).

Putting this Together to formulate your Clinical Impression:

• After looking at the ECG in Figure-1 — my thoughts were that we needed to know more about this patient! I saw sinus rhythm — a prolonged QTc — definite LVH by voltage — and, ST segment straightening + flattening (and slight ST depression) + T waves in multiple leads that strongly suggested hyperkalemia.
• The fact that the QTc is prolonged in association with hyperkalemia should suggest that there may also be hypocalcemia (these 2 electrolyte abnormalities in patients with renal disease so often go hand-in-hand). Although sensitivity and specificity of the ECG is far from optimal for detection of hypocalcemia — the morphologic picture we see here (ie, with fairly straightened but not elevated ST segments, at the end of which appears a hyperkalemia-looking T wave) should strongly suggest this possibility, especially in a patient with severe renal disease.
• NOTE — Marked LVH is very common in chronic dialysis patients. The reason why T waves in ECG #1 are not all that tall in multiple leads — and why ST-T wave changes typical for LV “strain” are not seen — might be that these 2 conditions are each attenuating ST-T wave effects of the other (ie, IF on a “baseline” of marked LVH + “strain”, serum K+ then becomes markedly elevated — then you might see exactly the ST-T wave pattern we see here in Figure-1, in which there is diffuse ST straightening with slight lateral ST depression + relatively modest T wave height in most leads given the high K+ value = 6.3 mEq/L).
• P.S. — Very important point emphasized by Dr. Smith! — when going back in the patient’s chart to look for prior tracings — BE SURE (as best you can) to determine the patient’s clinical status at the time the “baseline” tracing was done. This is why peaked and pointed T waves looked “unchanged” from the first prior tracing in this case — when the patient’s serum K+ was also high ( = 6.6 mEq/L) at that time.

Figure-2: The user-friendly criteria I favor for ECG diagnosisof LVH (For my source —  CLICK HERE).

A 20-something male with acute chest pain

I was texted this ECG with the words "sudden onset CP in a 20-something":

What do you think?

This was my response:

"This is abnormal in lateral leads. It probably is a normal variant but I would get a stat echo.

It is out of the bounds of the usual with normal variant because the ST Elevation is so focal to the lateral wall. Most normal variant has as much inferior STE as lateral (and of course without ST depression in aVL).  This is myocarditis versus myocardial infarction. He should get an immediate echo.  Problem is, even myocarditis will have a wall motion abnormality. And then the only way to tell rapidly is with an angiogram.  So if there is a wall motion abnormality, go to the Cath Lab.  Diagnosis will still probably be myocarditis."

I didn't realize it at the time, but this was the 2nd ECG.

Let's go back to time zero:

There was less ST elevation on this one.

Unbeknownst to me, the first troponin I had already returned elevated to 3.0 ng/mL by the time I received the text.


Here is more history:

The patient had an acute onset of epigastric and chest pain this morning. He was in 9/10 pain that last over an hour and did not improve with repositioning.

There was a repeat ECG at 70 minutes (the one texted to me)

There is increased STE in V4-V6.

Here is the echo report:

The estimated left ventricular ejection fraction is 53 %.  Normal left ventricular cavity size.

Regional wall motion abnormality-distal septum anterior and apex, posterior segment, small.

So the patient went for angiogram:

Coronaries were clean.

Here is the ECG recorded after the angiogram:

An MRI was done:

Impression:

1) Decreased LV function with apical wall motion abnormality
2) Normal dimensions of all cardiac chambers
3) Delayed gadolinium enhancement involving the distal inferolateral wall
with subendocardial sparing. Findings are most compatible with
inflammatory etiology such as myocarditis.

Learning points:

Myocarditis can exactly mimic OMI, including having a focal wall motion abnormality.  One usually just needs to take a look with angiogram in these cases.

In case you think that 20-somethings don't get coronary occlusion (OMI), think again:

24 yo woman with chest pain: Is this STEMI? Pericarditis? Beware a negative Bedside ultrasound.

A 16 year old girl has syncope while playing basketball.....

Chest Pain in a Male in his 20's; Inferior ST elevation: Inferior lead "early repol" diagnosed. Is it?

And another interesting case of myocarditis in a 20-something woman:

A Young Woman with Chest Pressure and Subtle, Focal ST Elevation/Depression

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Comment by KEN GRAUER, MD (6/11/2019):

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I LOVE this case — because it is both challenging and demonstrative of many important points.

• As always — I strive to maximize my objectivity as commenter by NOT reading what happened until after I commit to an interpretation of the ECGs in the case.

A total of 3 ECGs were done in this case.

• The 1st ECG shown above — was the ECG that was texted to Dr. Smith with the words, “Sudden onset of chest pain in a 20-something year old male”.
• The 2nd ECG shown above — was the initial ECG that was done in the ED on this patient. This ECG was done 70 minutes earlier.
• The 3rd ECG shown above — is the same as the 1st ECG shown above.
• The 4th ECG shown above — is the ECG that was done after cardiac cath.

For clarity — I have rearranged these 3 ECGs and numbered them ( = ECGs #1, #2, #3) in the sequence that they were done (Figure-1).

Figure-1: The 3 ECGs in this case in the sequence that they were done (See text).

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MY Thoughts on these Tracings: I began by first looking at ECG #2 — which is the ECG that was texted to Dr. Smith. As was the case for Dr. Smith, all I knew at the time — was that ECG #2 was obtained from a 20-something male with sudden onset of chest pain.

• I interpreted ECG #2 as showing — sinus rhythm — normal intervals (PR/QRS/QT) and normal axis (about +70 degrees) — no chamber enlargement — small lateral (normal septal) q waves — normal R wave progression (with transition between leads V2-to-V3) — and ST elevation in the infero-lateral leads.
• The shape of the elevated ST segments was concave-up (ie, “smiley”-configuration) — with J-point notching in leads V4 and V5. Most of the time — this ST-T wave morphology will be associated with a benign repolarization variant when seen in a 20-something year old male ...
• Looking closer — the amount of ST elevation in leads V5 and V6 seemed a bit more than what is usually seen with benign repolarization variants. That said, in view of normal-appearing ST-T wave morphology (ie, concave-up ST elevation with J-point notching) + normal R wave progression with a relatively short QTc + lack of reciprocal ST depression + the patient’s young adult age — I thought ECG #2 was most likely to reflect a repolarization variant.
• That said — I wanted to know more about this patient before rendering a final interpretation ...

At this point, we learned that ECG #2 was not the initial ECG done on this patient. Instead — the initial ECG was ECG #1, which was done ~70 minutes before ECG #2. I compared these 2 tracings:

• There is artifact in several leads of ECG #1 — but otherwise, ECG #1 and ECG #2 are quite suitable for comparison purposes, because there is no appreciable change in frontal plane axis — and no more than minimal change in chest lead QRS morphology.
• I saw slightly less ST elevation in leads V5 and V6 in the Time = 0 Tracing ( = ECG #1) — BUT — I thought T wave peaking and relative T wave size (compared to the QRS in the same lead) was more in leads I, V3 and V4 in the initial ECG ( = ECG #1) compared to the later ECG ( = ECG #2).
• I definitely wanted to know more about this patient … As per Dr. Smith — the differential diagnosis included: i) A repolarization variant; ii) Acute MI; and, iii) Acute Myocarditis (or Myopericarditis).

At this point — we were told that the 1st troponin had returned elevated to 3.0 ng/mL — and — we were given the additional history that the patient’s chest pain was severe (9/10) lasting over an hour, and not improved by repositioning.

• Echo revealed an EF = 53% + regional wall abnormalities.
• Cardiac cath revealed normal coronaries.

We were then shown ECG #3, done after cardiac cath. Comparing the 3 ECGs in Figure-1 in the sequence the were obtained — it should now be obvious that ECG #3 shows ST-T wave abnormalities clearly consistent with the diagnosis of acute MyoPericarditis:

• There is more ST elevation than-there-should-be in leads V4-thru-V6.
• The T wave in neighboring lead V3 looks disproportionately tall compared to R wave amplitude in this lead.
• There is NO doubt in ECG #3, that the T wave in lead I is hyperacute and associated with more ST elevation than should be seen in this lead with this tiny of a QRS complex. ST-T wave appearance in lead I of ECG #3 clearly looks more worrisome than it did in ECG #2.
• The T wave in lead aVL has become upright in ECG #3 (even though tiny — the T in aVL was flat in both ECGs #1 and #2).
• Putting It All Together — the findings we see in ECG #3 are consistent with acute MyoPericarditis = ST elevation with T wave peaking in multiple leads (Right-sided leads aVR and V1 typically do not manifest ST elevation with pericarditis) + the finding that the abnormal ST-T wave appearance in lead II looks much more like lead I than lead III (with acute inferior MI — it is leads II and III that tend to show similar ST-T wave changes).

My LEARNING Points:

• The usual differential diagnosis for ST elevation in a younger adult includes: i) A repolarization variant; ii) Acute MI; and, iii) Acute Pericarditis (or Myocarditis or Myopericarditis). Sometimes distinction between these 3 entities may be quite difficult when all that one has is a single ECG and a history of “chest pain”. I initially favored a diagnosis of “probable repolarization variant” in this case when all I had to look at was ECG #2.
• History is KEY. Even marked ST elevation is often benign when a young adult is either asymptomatic or presents with atypical symptoms. On the other hand — the severe new-onset chest pain in this case was clear indication of a need for more information + diagnostic testing (ie, stat Echo, troponin, repeat ECGs). Once known that serum troponin was definitely elevated — I knew the ECGs were not simply a repolarization variant ...
• Considering the serial tracings shown in Figure-1 — the ECG findings + the wall motion abnormalities and elevated troponin are all consistent with acute Myopericarditis.

A patient with chest pain that is resolving. Computer interprets ED ECG as completely Normal.

I posted this case a long time ago, before I started ranting about ECGs that are called completely normal by the computer.

A 60-something with chest pain arrived to the ED by ambulance with resolving chest pain.  Here is his ED ECG:

The computer interpretation was:
"Normal ECG"
What do you think?

This ECG is NOT normal.  The T-waves in V2-V4 are very large in proportion to the QRS.   They are suspicious for hyperacute T-waves. There is low QRS amplitude.   

This points out another interesting phenomenon: hyperacute T-wave occur "on the way up" (before ST elevation, as the ST is on its way up) but also "on the way down" (when there is reperfusion, either spontaneous or by therapy): the ST segments may normalize before the T-wave normalizes, so that there are residual hyperacute T-waves.

Can you trust a computer interpretation of "normal?" 

Clearly not!  Here are 24 examples of critical ECGs that were called "normal" by the computer.

1. Hughes KE et al. Safety of Computer Interpretation of Normal Triage Electrocardiograms. Acad Emerg Med 2017; 24(1): 120 – 24. PMID: 27519772

This study, discussed on Salim Rezaie's fine site REBEL EM, implies you can trust the computer interpretation of "normal." (http://rebelem.com/triage-ecgs-reducing-interruptions-busy-ed/)

We recently wrote an editorial debunking this study: 

Litell, John M., H. Pendell Meyers, and Stephen W. Smith. 2019. “Emergency Physicians Should Be Shown All Triage ECGs, Even Those with a Computer Interpretation of ‘Normal.’” Journal of Electrocardiology 54 (March): 79–81. https://doi.org/10.1016/j.jelectrocard.2019.03.003.

What to do?

Recording serial ECGs would be useful.  The chest pain is resolving, so if these are resolving hyperacute T-waves, then followup ECGs should show their size diminishing.

However, when I saw this patient, I knew that he had come by ambulance, so I knew there must be a prehospital ECG recorded somewhere and went to look for it. 

I found it. 

Here it is:

Need I say more?
Yes, I'll say more: see the computer interpretation:
"Normal variant ST elevation, consider early (repolarization)"
Why the medics did not see it, I'm not sure. 

The cath lab was activated, as it should be with transient STEMI. 

See this case of transient STEMI:

Spontaneous Reperfusion and Re-occlusion - My Bad Thinking Contributes to a Death.

Angiogram: There was 80% obstruction of the LAD with a large thrombus and TIMI-2 flow; the thrombus was suctioned out.

All serial troponins were undetectable!  (Remember this the next time you think you have ruled out a patient without looking at all the ECGs)

Comment:
Had we not seen those subtle hyperacute T-waves, and then sought out the prehospital ECG, the patient would have ruled out, with one of three outcomes:

1. Subsequent thrombus propagation with re-occlusion, recurrent chest pain and diagnosis made (although perhaps late and perhaps only after an adverse outcome)

2. Undergone stress test with uncertain results.

3. Been discharged to home with potential disastrous outcome.


Learning Points

1.  Computer algorithms that make the diagnosis of "normal" are usually correct, but is usually good enough?

2. Computer algorithms are completely unreliable at diagnosing STEMI, with both poor sensitivity and poor specificity.  Here are two recent articles confirming this:

    a. The Comparison of Physician to Computer Interpreted Electrocardiograms on ST-elevation Myocardial Infarction Door-to-balloon Times.
    b. Electrocardiographic diagnosis of ST segment elevation myocardial infarction: An evaluation of three automated interpretation algorithms

3.  Always look for the prehospital ECG

4.  Hyperacute T-waves occur not only shortly after onset of chest pain (as the ST segment is about to rise, or "on the way up"), but also shortly after reperfusion (as the ST segment is resolving after reperfusion or "on the way down").

5.  With very brief occlusions, troponins may all be negative.  What would high sensitivity troponins have shown?  We don't know.

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Comment by KEN GRAUER, MD (6/9/2019):

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As per Dr. Smith — this “repeat case” is clearly worth repeating! I’ll add several thoughts to the important points highlighted by Dr. Smith. To do so — I’ve highlighted key findings of the initial ECG in this case — and contrast this with the normal ECG that Dr. Smith posted a few days earlier on June 7 (Figure-1).

Figure-1: The initial ECG in the ED from this case ( = ECG #1) — contrasted with chest leads in the normal ECG taken from our June 7 Case  (See text).

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COMMENT on ECG #1: As always, the History is KEY to optimal ECG interpretation. The fact that this 60-something man presented with resolving (not ongoing! ) chest pain should clue us in to the fact even IF he has just had acute OMI, that ST segments may only be minimally (if at all) elevated. Instead, we are likely to see more of a reperfusion ST-T wave picture — or as in this case, hyperacute T waves“on the way down”.

Dr. Smith speaks at length in answer to the question as to whether you can “trust” a Computer Interpretation of an ECG as “normal”. I’ll address this issue by repeating what I wrote in My Comment on March 11, 2019 to a case Dr. Smith posted.

• In my opinion — it is not the fault of the computer that the diagnosis was missed. Instead — it is the fault of the provider who accepts the computer interpretation without independently interpreting the ECG before looking at what the computer said. My views may differ from others, in that as an Attending charged with overreading ECGs for numerous providers — I loved the computerized interpretation once I appreciated what the computer can and cannot do. That’s because the computer saved me LOTS of time (!) by speeding up my interpretation, when I would be confronted with a large stack of ECGs in front of me to interpret. But for anyone who has read less than many thousands of tracings — it is imperative not to even look at the computer interpretation until after YOU have independently interpreted the ECG yourself! Failure to follow this suggestion will most likely lead to overlooking a number of subtle acute MIs. NOTE: I expand on my approach to Optimal Use of Computerized ECG Reports — HERE —

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Back to ECG #1 in this Case: The reasons why I was immediately concerned about acute OMI on seeing ECG #1 were: i) The history of new-onset chest pain severe enough to summon EMS; ii) The hyperacute T waves in the chest leads; and, iii) The fact that no less than 11 out of the 12 leads on this ECG (ie, all leads except aVR) are abnormal!

• Clearly — i) and ii) are more than adequate for activating the cath lab — but, I think it important to get GOOD at recognizing ST-T wave abnormalities, even when they are not as flagrant as the hyperacute T waves in ECG #1.
• Proportionality — is the KEY word for appreciating that the T waves in leads V2-thru-V4 are hyperacute in view of the history of recent chest pain. T waves tower over the QRS complex in leads V2 and V3 — and, T wave amplitude in lead V4 still exceeds QRS amplitude in this lead.
• Neighboring Leads — is the KEY concept for appreciating that the T waves in leads V5 and V6 of ECG #1 are also hyperacute — since the Shape of these T waves is quite similar to T wave shape in leads V2-thru-V4. Even though T wave amplitude in leads V5 and V6 is less — their similar shape tells you this is part of the overall process. And, in the context of these T wave abnormalities in leads V2-thru-V6 — we can confidently say that the coved and slightly elevated ST segment in lead V1 is also abnormal!
• R Wave Progression — is telling in ECG #1, because there is no more than a minimal r wave in leads V1 and V2 — and, the R waves that subsequently form remain quite small through to lead V6. Compare the amplitude of these chest lead R waves in ECG #1 — with the prehospital ECG (shown above) — in which transition occurred by lead V2, with substantial R wave amplitude in the mid-chest leads. This loss of R wave is clearly the result of the large anterior STEMI that this patient has just had.
• ST Straightening — is the KEY word for appreciating that there are ST-T wave abnormalities in no less than 11 of the 12 leads in ECG #1. First — Note the shape of the normal ST-T waves in the chest leads of the June 7 Case (BOTTOM in Figure-1) — in which there is a gentle upsloping concavity to the ST segments, with imperceptible (smooth) transition between the end of the ST segment and the beginning of the T wave. Contrast this with distinct ST Segment Straightening in leads I, II, aVL, aVF; and V2-thru-V6 (parallel RED lines in ECG #1). In addition, this ST straightening in leads V5,V6 manifests an abrupt angulation at the ST segment-T wave juncture.
• Finally — there is the coved ST segment with shallow T wave inversion in lead III. By itself, in association with the predominantly negative QRS complex in this lead — this might not be an abnormal finding. But in the context of definite ST segment straightening in neighboring inferior leads II and aVF — the ST-T wave in lead III must be assumed as part of the overall picture.