A 60-something who has non-specific generalized malaise and is ill appearing.

An anonymous paramedic sent this.

A 60-something with past history only of colon cancer called 911 for non-specific generalized malaise.

The medics state that he was ill appearing.

They recorded an ECG:

What do you think?

This is extremely wide, and even if it is VT, it is so wide that there must be hyperkalemia or a severe Na channel blocking overdose.  The patient was not on a sodium channel blocker.

The paramedic knew instantly what it was (he credits his regular reading of this blog!)

The patient was only a couple blocks from the hospital, so there was no time for treatment before arrival.

K was 8.9 mEq/L.

Etiology was a combination of NSAID and obstructive nephropathy, with a Cr > 20 (!).  Estimated GFR of 2.0.

The potassium was brought down and the patient ultimately did well.

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

This is a very commonly missed ECG of a terrible condition.  In this case, it was almost dismissed.  I present many other similar ECGs at the bottom that were indeed missed or dismissed.


Case

I was texted this ECG from a physician assistant who works by himself in several small Emergency Departments.

He is a particularly smart and well trained emergency medicine PA (because he trained at Hennepin).

He added the words:

"What do you think?  70-something male with DM, HTN, no previous MI, with Chest pain"

What do you think?

Here was my response:

"Definite Huge Occlusion MI (OMI). STEMI! This is a bad one.  There is RBBB with Left Anterior Fascicular Block (LAFB) which is a very ominous sign."

He texted back:

"That's what I thought but the cardiologist (at the receiving facility) was not convinced."

This is an obvious diagnosis to me.  Unambiguous.  Can't be anything else.
There is RBBB with LAFB with huge ST Elevation seen in V2-V4, (also subtle STE in aVL).

(The rhythm is uncertain, but it is supraventricular and probably atrial bigeminy (with P-waves that are not well seen), but the rhythm diagnosis is NOT critical in making the OMI diagnosis.)

Here I have put a line at the end of the QRS and beginning of the ST segment, so that you can assess for ST Elevation:

The image is distorted because it was a photo of a paper ECG.  
That is why the lines are not parallel.
Note that the QRS itself can mimic ST deviation; this is especially seen in inferior lead here.

Also note that the Elevated ST Segments in V2 and V3 are downsloping.  In the many cases of RBBB + LAFB in anterior MI that I have seen, this is the rule rather than the exception.  

Case continued:

The PA transferred the patient and, on arrival, the ECG was reportedly even more obvious.  The patient went to the cath lab:

Proximal LAD: 90% with thrombus
Mid LAD: 80% with thrombus
Distal LAD: 80% with thrombus

3 stents were placed.  Peak hs Troponin T was 23,070 ng/L (equivalent to 23 ng/mL; this is an enormous infarct!).

Echo showed anterolateral and septal wall motion abnormalities and an ejection fraction of 29%.

Comment:

Some ECG findings which are very clear to me are not clear to others.  I try not to post cases that are easy.  This one I would have thought was easy.  But apparently it is not, as ECGs like this are very often missed, by all kinds of providers, including cardiologists.



More similar cases

Other examples of RBBB/LAFB OMI in which the cardiologist contradicted the interpretation of the emergency provider and disagreed with cath lab activation:

I had just resuscitated this patient from VF cardiac arrest after 68 minutes of CPR:

I told the cardiologist that it is a proximal LAD occlusion and he rolled his eyes, and said "Maybe."  It was indeed acute LAD OMI

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

____________________________

Here is another example in which the cath lab was activated, then de-activated by the cardiologists, with the ST Elevation annotated below it:

This patient died 8 hours after cath lab de-activation.

With markup

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

_________________________

Here is another that was missed:

Resuscitated from ventricular fibrillation: what is the ECG Diagnosis?

________________________

Finally, this one

Here is a case of a young woman who presented with acute pulmonary edema.  The ECG was recorded during the pulmonary edema.  Cath lab was activated, then she arrested, and, after 30 minutes of resuscitation, achieved ROSC but was in severe shock.

Sinus tachycardia (NOT VT!).  See P-waves in lead II across the bottom.
RBBB and LAFB (wide complex)
There is clear STE in aVL, V2, and V3.
There is deep reciprocal ST depression in II, III, aVF.

The cath lab was de-activated.  She died of a 100% left main occlusion and peak troponin I of 500 ng/mL (the highest troponin I have ever heard of).

___________________________

Here is another that was missed by the ED providers:

This is a patient with chest pain and the following prehospital ECG:

Here are lines that mark the end of the QRS and beginning of the ST segment:

This also has RBBB and LAFB with ST Elevation, but more subtle
This STEMI was not recognized and the patient arrested and could not be resuscitated.

Learning Points:

1.  Level of training does not predict ability to diagnose OMI from the ECG. Paramedics and PA's can be outstanding at this.

2.  Beware RBBB with LAFB.  ST Elevation may not be obvious, or it may be.  It does distort the ECG and it confuses many ECG interpreters.

"Long QT" after droperidol

A patient presented to the ED with intractable hiccups.  He also had "ongoing GERD symptoms with heartburn......but no chest pain"  (Whatever that means).  He was treated with droperidol and benadryl and this decreased his symptoms and he was discharged.  No ECG was recorded (!).

Later, the patient returned with altered mental status and reports of falls.

He had an ECG recorded:

The QT was 504 ms
The computerized QTc (Hodges correction) was listed as 530 ms.
Bazett correction would be 563 ms
The providers were worried that the droperidol had resulted in a long QT.
What do you think?
See below for explanation.

There are huge U-waves, best seen in V1-V3.  These are almost always due to hypokalemia.  Some overdoses can cause this:

Cole JB, Stellpflug SJ, Smith SW: Refractory Hypotension and “Ventricular Fibrillation” With Large U Waves After Overdose (this is a great full text online case of hydroxycholorquine overdose)

Here I have drawn lines at the beginning and end of the U-waves in V1-V3
Then I draw them down to lead II across the bottom
Then I go to sections that are under I-III, aVR-aVF, and V4-V6.
Then I draw the line up through those leads to show where the U-wave is in those leads.
And you can see how what may appear to be a T-wave and a long QT is really a U-wave.
V4-V6 in particular show only one wave which appears to be a T-wave only.  But by showing from other leads where the U-wave vs. T-wave is, we can see that this apparent T-wave is really a U-wave.

Whether it is a long QT or a QU, it may be equally prone to ventricular tachycardia and VF.
However, the etiology of U-waves is different is different from the etiology of long QT.
This would not be drug effect due to droperidol, but more likely hypokalemia.

The K was measured and was 1.7 mEq/L

Learning Points:

1.  When the QT seems impossibly long, consider that it might be U-waves which are mimicking long QT (often with a long QU interval)

The etiologies of long QT and large U-waves are different, even if they both may have the same dysrhythmic consequences.  Therefore, the treatment will be different.

2. Also, patients with intractable hiccups, or who have what they call "heartburn", should usually get at least an ECG, as ischemia could be underlying both of these.

Bizarre T-wave inversions, with Negative U-waves and Very long QT. And a myocardial viability study.

This 60-something year old male was admitted and his hospital course complicated by GI bleed, hemodynamic instability, and a nadir hemoglobin less than 5 g/dL.  An ECG was relatively normal.

The next AM, his potassium was measured at 2.9 mEq/L, so another ECG was recorded.

He was asymptomatic.

The previous ECG from one week prior had been relatively normal.

There are bizarre inverted T-waves and also inverted U-waves (see the 2nd inverted bump?)
The QT is incredibly long
There is some subtle STE in inferior leads but also STE in I, aVL.
There is STE before the bizarre TU inversion in leads V3-V6.

There are some artifacts that look similar to this.  

Bizarre (Hyperacute??) T-waves

Inverted U-waves are very strongly associated with LAD occlusion.

Besides the Nonspecific T-wave Inversion in aVL, What Else is Abnormal on this ECG?

Bizarre T-wave inversion with long QT is typical of takotsubo.

Bizarre T-wave Inversions in a Patient without Chest Pain

I thought he either had acute MI of the LAD, or takotsubo stress cardiomyopathy.  The team obtained an immediate cardiology consult, a stat formal echo, and serial troponins.

Troponin I was 4.2 ng/mL.
Echo showed: 
Low normal left ventricular systolic function with an ejection fraction of 52%.

Regional wall motion abnormality--akinesis of the apical anterior, mid-anteroseptal, apical septal, apical inferior, and apical lateral segments.

Regional wall motion abnormality--hypokinesis of the mid anterolateral and anterior segments.

Hyperdynamic basal segments.

This is consistent w/ wraparound LAD occlusion or takotsubo; the ECG is consistent with both.

Cardiology consult elicited some brief episodes of chest pain while in the hospital, squeezing, lasting 10 minutes.

The patient went for an angiogram.

Impression and recommendation:
Severe multivessel CAD involving the ostial LAD.
Occlusion of the apical LAD resulting in inferior infarction, chronicity uncertain - decreasing troponin would suggest that occlusion is more than 24-48 hours old.

Given the distal LAD occlusion of uncertain chronicity, TIMI III flow in other vessels and patient restlessness, as above, intervention was deferred.

Here is the ECG after the angiogram:

Some interesting evolution

After all this, it was not certain whether there was ACS (type I MI), type II MI due to GI bleed with anemia and hemodynamic instability, or takotsubo.

Further, if it was MI, was it:
1) a large MI with downtrending troponin or
2) a previous large MI due to the previous LAD occlusion, with superimposed small acute MI, or
3) a small acute MI with a large area of myocardial stunning (large wall motion abnormality)?

Absence of Q-waves on the ECG should argue strongly against a large irreversible infarction.  This was almost certainly a small infarction or takotsubo.

A Thallium Myocardial Viability Study was done.

--Myocardium may not contract because of "hibernation" or stunning, which are reversible, as well as by irreversible infarction.
--This may be assessed by Thallium scintigram myocardial viability study.
--Details of this are beyond the scope of this article, but may be found here (full text, 2019).

FINDINGS:
Review of the rest/redistribution 3 plane SPECT reconstructed scintigram demonstrate normal perfusion on the immediate scintigram except for a small area of reduced perfusion in the apical inferior and mid segments consistent with absence of infarct and normal viability in all vascular
distribution. The 24-hour/redistribution image shows reduced uptake in the apical and mid inferior wall adjustment to significant subdiaphragmatic tracer uptake most consistent with ramp filter artifact.

Impressions:
1. Normal viability of the anterior, anterolateral, septal, and inferolateral walls.
2. High probability of viability in the inferior wall.

This answered the above questions:

Thus, it was not a large infarction with downtrending troponins, or an old infarction with acute MI superimposed.

It had to be either a small infarction (type 1 or type 2), or takotsubo.  And this is evident from the ECG.

What does this ECG with significant ST Elevation represent?

These 2 serial ECGs were texted to me recently.  They were recorded 12 minutes apart:

"Hey Steve, 30-something with one week of chest pain, mostly right-sided, better with sitting up.":

What do you think?

QTc's were 330 ms and 373 ms

This is what I texted back:

These look like they are a very pronounced case of Benign T-wave Inversion.  I do not think this is acute occlusion myocardial infarction (OMI).  Get an emergent contrast echocardiogram.

These are reasons why it does not look like OMI: 

1. flat ST segment in V4

2. huge R-wave in V4

3. very short QT interval

4. J-point notching

5. classic early repol in V3

6. classic features of “Benign T-wave inversion” T-waves in V5, V6.  

I would guess the patient is African American.

Would I blow it off?  No.  I would get an echo.  I am 99% certain that it is not OMI.

An emergent echo was done:

Normal left ventricular size, normal wall thickness and mild to moderate systolic dysfunction.

The estimated left ventricular ejection fraction is 43%.

Global hypokinesis.

The first troponin I then returned quite elevated at 9.8 ng/mL.

In the absence of a wall motion abnormality, especially with global decreased ejection fraction, a troponin that is quite elevated like this strongly suggests global myocarditis.  

When does myocarditis mimic OMI?  Often, myocarditis is more focal, has both focal ST Elevation and focal wall motion abnormalities, as well as elevated troponin, and an emergent angiogram must be done to differentiate the two entities.  Definitive diagnosis is by MRI.

I learned more about the history:

30-something African American with 5-7days of sharp R-sided shoulder/scapula/chest discomfort, presented with sinus tachycardia.  This history of a week of constant chest pain is also much more suggestive of myocarditis.  

OMI is generally of more acute onset, unless there is intermittent angina.  OMI it is very unlikely with a week of constant pain.

2 hours later, this ECG was recorded:

This was interpreted as having Wellens'-like reperfusion T-waves.
I would have said they were also likely due to different lead placement or to common hour-to-hour variation in non-ischemic ST elevation.

However, to be certain, the patient went for an angiogram.

Angiogram was normal

C-reactive protein (CRP) returned at 250 mg/L, consistent with myocarditis.

Serial Troponins remained in the 9-11 range, w/o any large rise and/or fall, also atypical for OMI.

He later underwent an MRI:

1) Mildly decreased LV function with no focal wall motion abnormalities
2) Patchy intramyocardial delayed enhancement compatible with myocarditis.
There is also mild pericardial enhancement consistent with pericarditis.
Overall findings are consistent with myopericarditis.

One month later,  a convalescent ECG was recorded:

The typical benign T-wave inversion is still present.  But the significant ST Elevation is resolved.

Thus, that STE was due to myo-(peri)carditis.

Summary:

It was not benign T-wave inversion, but also not OMI.

When there is worry for OMI, but the ECG and history are just not right, then an emergent contrast echo may be done in lieu of an immediate angiogram.

A wall motion abnormality and elevated troponin may be seen in myocarditis, and then an angiogram must be done to differentiate myocarditis from OMI.

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Comment by KEN GRAUER, MD (7/21/2019):

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This case raises interesting issues relating to HOW to interpret the initial ECG ( = ECG #1 in Figure-1). The patient is a 30-ish year old man, who presented to the ED with a 1-week history of chest pain that was mostly right-sided — and improved with sitting up.

• The ECG was repeated 12 minutes later ( = ECG #2).
• A 3rd ECG was recorded 2 hours later ( = ECG #3).

Additional subtle teaching points arise with close examination of the serial ECGs in this case.

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

THOUGHTS: As I suggested in My Comment to Dr. Smith’s Case from July 19 —  An optimal way to enhance one’s ECG interpretation skills is to always interpret the initial tracing in the context of the brief clinical history given (which in this case, was 1 week of right-sided, positional chest pain in a 30-ish year old man).

• Interpret this initial ECG before you look at additional information (or additional tracings). THEN reconsider your interpretation in the context of whatever additional information you are able to obtain.

Dr. Smith emphasized the KEY point regarding the interpretation of ECG #1 — namely that in view of the history of this patient, these ECG findings are unlikely to reflect acute OMI.

• In addition to the reasons cited above by Dr. Smith against ECG #1 being acute OMI — I would add: i) Upward-sloping ST segments in the leads with the most ST elevation (leads V3, V4); ii) Lack of reciprocal ST depression; iii) Lack of significant Q waves (I believe there is an rSr’ complex in lead aVL); and, iv) The atypical history. Of course, none of these features are definitive — and, as per Dr Smith — emergent Echo + ongoing clinical correlation are essential for attaining maximal certainty that this is not acute OMI.
• A NOTE on the History: When (as occurs in this case) — the patient is a younger adult and, the history is atypical for acute MI (ie, right-sided location; pleuritic and/or positional component to the chest pain) — then the prevalence of acute myocarditis as a diagnostic possibility increases significantly.

So, I did not think that ECG #1 was the result of acute OMI. I also thought this tracing looked unusual for a benign T wave inversion repolarization variant ( = my opinion).

• In my experience — Benign T wave inversion in younger adults is almost always associated with ST segment coving and elevation with T wave inversion that is especially prominent in anterior leads. I’m not used to seeing significant T wave inversion in leads V5 and V6 in benign variants, without seeing any of this in leads V2 and V3. On the other hand — acute myocarditis may present with ECG changes localized to a number of contiguous leads in a pattern less typical for acute OMI or benign repolarization.
• The beauty of troponin and Echo in the ED for cases like this — is that it can rule out benign variant when abnormal results are obtained. As per Dr. Smith — definitive diagnosis was obtained later in this case after cardiac cath and MRI.

Other Interesting ECG Features:

QUESTION: Look at ECG #2 in Figure-1. Does the extra ST elevation we now see in lead V3 reflect progression of acute ischemic changes?

ANSWER: I do not believe there is any significant change between ECG #1 and ECG #2. The limb leads are virtually identical in both tracings. The major difference in the chest leads — is that transition now occurs much sooner in ECG #2 (the R wave is predominant already by lead V3 — whereas transition did not occur in ECG #1 until lead V4). As a result — the shape and relative amount of ST elevation in lead V3 of ECG #2 — is comparable to what we see in lead V4 of ECG #1.

• Instead — I believe lead V2 in ECG #2 is malpositioned because: i) There is actually a terminal r’ in lead V2 that should not be there, especially since there was no terminal positive deflection (no r’) in lead V1; and, ii) It does not make physiologic sense for the T wave in ECG #2 to manifest a 3mm positive deflection in lead V1 — then a barely positive T wave in lead V2 — and, then a markedly positive ST-T wave by lead V3.
• PEARL: When you are depending on being able to pick up fine serial ST-T wave changes between successive ECGs — you may want to consider marking the patient’s chest to ensure similar lead placement for serial tracings. Doing so would have avoided the confusion we are confronted with for assessing chest lead progression in ECG #2.

QUESTION: What about ECG #3 in Figure-1? Was it wrong to consider Wellens’-like reperfusion T waves, given the change in lead V3’s appearance?

ANSWER: Even when the chest is marked to ensure consistent precordial lead placement — there may still be slight tracing-to-tracing variation in QRS morphology and amplitude. Sometimes — this just happens. As a result — judgement is needed when interpreting serial tracings:

• I have no “magic formula” for when to say that the difference between one ECG and the next is due to lead placement variation or axis change — vs — a TRUE significant ST-T wave change due to an acutely evolving infarct. Instead — one develops a “judgment Gestalt” from looking at numerous tracings, and then correlating your impressions by subsequent ECGs and what happened to the patient.
• NOTE: Frontal plane Axis may vary depending on the patient’s position in bed (ie, whether the patient is flat in bed — or to a certain extent inclined due to increased dyspnea when the bed is flat). It is important to appreciate that a change in frontal plane axis may sometimes dramatically alter QRS morphology and resultant ST-T wave appearance. That said — this is not a factor in Figure-1 — since both QRS morphology and frontal plane axis in the limb leads of all 3 ECGs is virtually identical!
• Did YOU notice? — that ECG #3 again shows return to a predominant S wave in lead V3 (whereas the R wave was predominant in lead V3 of ECG #2). This observation suggested to me that for comparison purposes of ST-T wave changes in the chest leads for the 3 ECGs shown in Figure-1 — we should be using ECG #1 and ECG #3 (but not ECG #2).
• Despite the fact that in ECG #3 — lead V3 now shows ST segment coving and fairly deep T wave inversion (that was not seen in ECG #1) — I did not think this was an acute ischemic change because: i) This change is really only seen in a single lead (lead V3); ii) Lead V3 in ECG #3 to me looks like the “natural result” of being a “transition lead” between what we see in leads V2 and V4 of ECG #3; and, iii) I thought the localized ST-T wave findings with little change over 2 hours in this younger adult with symptoms atypical for acute MI was much more consistent with acute myocarditis.

Our THANKS to Dr. Smith for this interesting case!

A man in his 40s with chest pain and syncope after cocaine use

Written by Pendell Meyers, with edits by Steve Smith


A man in his early 40s with history of MI s/p PCI presented with bilateral anterior chest pain described as burning and belching with no radiation since last night starting around 11pm (roughly 11 hours ago). He also described a syncopal episode just prior to onset of symptoms. He had used cocaine approximately 20 minutes prior to onset of symptoms.

He still had active pain on arrival to the ED.

Here is his triage ECG:

What do you think?

His baseline ECG was on file:

--Sinus rhythm

--Subtle STE in V1-V5, II, III, and aVF

--Q-waves in V1-V5, as well as II, III, and aVF which must be assumed new until proven otherwise

--Possibly large area under the T-wave (concern for hyperacute T-waves) in V4, II, III, and aVF, with reciprocal negative T-wave in aVL

--These Q-waves are so fully developed that it appears to be a nearly completed MI, at a stage when it is likely that all ST elevation is resolved. STE occurs primarily in viable ischemic myocardium; persistent STE after completed infarction is ominous and portends development of an aneurysm.

--There is also an interesting Brugada-like morphology in V1 (also similar to hyperkalemia, which sometimes mimics brugada). This morphology can be cause by or associated with cocaine:

A Patient with Cocaine Chest Pain and Prehospital Computer interpretation of ***STEMI***

This is OMI of the anterior, lateral, and inferior walls until proven otherwise. This distribution is classic for a type III "wraparound" LAD Occlusion.

But it does not meet STEMI criteria and it was not initially recognized. Whereas most STEMI(-) OMI is acute, this one might have had STE at its onset, or earlier in its course. We'll simply never know without ECGs from that time period.

The first troponin T was delayed for several hours for an unknown reason in the lab, and returned at 1.50 ng/mL (very elevated).

This prompted a repeat ECG (we do not have documentation from that time to tell us whether he had persistent, recurrent, or absent pain):  

Progression of anterior OMI to full Q-wave MI with large pathologic Q-waves in V2-V4 with persistent STE which now meets STEMI criteria (after full thickness infarction/stunning).



The cath lab was now activated.

He was found to have 100% mid LAD occlusion. Thrombectomy performed, then stent placed with improvement of TIMI 0 to TIMI 3 flow.

Pre-PCI:

Post-PCI:

In this view you can see the extent of the "wraparound" distal LAD:

Peak troponin T was 35.70 (massive MI, rarely survivors at this level in my 3 years here).

Echo showed EF 30% with anterior, septal, apical, and inferior wall motion abnormalities.

ECG after cath:


Continued STE with anterior wall Q waves (LV aneurysm morphology), combined with extremely high troponin are likely indicative of full thickness irreversible MI (rather than stunning), and are high risk features for resulting LV aneursym. The extremely high troponin and ECG evidence of LVA morphology are very worrisome long term features for resultant morbidity and mortality.

Amazingly, he did not suffer any serious complication in hospital. He recovered and was discharged several days later. Long term follow up is unknown at this point.


Learning Points:

Even if NSTEMI Occlusions (STEMI- OMIs), overall prove to have slightly lower morbidity and mortality than STEMI Occlusions (STEMI+ OMI), there are many cases like this one showing that some of the worst, largest OMIs may not manifest STEMI criteria until far too late, if ever. Again, it is possible that this patient would have had obvious STE earlier in the time course of this MI, but we do not know. What we can say is that his initial ECG was certainly diagnostic and the delay of many hours could have been improved.

Wraparound type 3 LAD Occlusion causes STE in many leads including anterior, lateral, and inferior distributions. This is the most important exception to the classic teaching of "diffuse STE without reciprocal depression is less likely ACS, more likely pericarditis". Always keep in mind the possibility of diffuse STE (and other OMI findings) as being due to a type 3 LAD.

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Comment by KEN GRAUER, MD (7/19/2019):

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I was intrigued by the challenge of clinical correlation posed by the ECGs in this case. The patient is a man in his 40s with a history of prior MI (s/p PCI) — who presented to the ED with new chest pain that had begun ~11 hours earlier. His initial ECG in the ED ( = ECG #1) is shown in Figure-1. The patient was still with ongoing chest pain at the time ECG #1 was done.

• A baseline tracing was found on this patient ( = ECG #2).
• Several hours later a follow-up ECG was obtained in the ED, because the 1st troponin came back significantly elevated ( = ECG #3).

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

CHALLENGE: How did YOU interpret ECG #1 before you looked at ECG #2?

• As we soon learned in this case — this patient has had a new STEMI. Cardiac cath (which was done soon after ECG #3) told us that this STEMI was the result of 100% mid-LAD occlusion (LAD with wraparound). But the BEST way to enhance one’s ECG interpretation skills is to always interpret the initial tracing in the context of the brief clinical history given (which in this case, was new chest pain that began 11 hours earlier).
• Strive to interpret this initial ECG before you look at additional information. THEN look for previous tracings in the patient’s chart, repeat ECGs, troponin and Echo results + the patient’s clinical course. This sequence of assessment will not slow you down — and it is the BEST way to optimally “grow” as an astute ECG interpreter.

My THOUGHTS on ECG #1 (determined BEFORE I looked at ECG #2):

Remember the History = a man in his 40s with known prior MI (s/p PCI) — who presented to the ED with new chest pain that had begun ~11 hours before ECG #1 was done.

Descriptive Analysis of ECG #1:

• The rhythm is sinus at a fairly regular rate of ~80-85/minute. The PR, QRS and QTc intervals are all normal. The frontal plane axis appears to be normal — though the axis is difficult to calculate because of nearly isoelectric complexes in 4 of the 6 limb leads (leads I, III, aVL and aVF). There is no chamber enlargement.

Regarding Q-R-S-T Changes:

• There are multiple Q waves in ECG #1. Although small in size — the inferior Q waves are likely to be significant (ie, indicative of inferior MI at some point in time) — because relative to QRS dimensions, inferior Q waves are both large and relatively widened. There are large Q waves (relative to QRS complex size) in leads V1, V2 and V3. There is marked fragmentation of the QS complex in lead V3.
• PEARL: Although Q waves in leads V4, V5 and V6 become much smaller and narrower — the fact that the Q wave in lead V4 is decidedly larger than the Q waves in leads V5 and V6, tells us that the Q in V4 is significant (ie, part of the infarction process suggested by the Q waves in V1-V3). With normal “septal” q waves — the opposite progression occurs (ie, Septal q waves are uncommon in lead V4 — and when present, a septal Q in V4 should be smaller than the septal Q in V5 and V6).
• The area of Transition (ie, where the R wave becomes taller than the S wave is deep) is slightly delayed in ECG #1 (ie, it occurs between leads V4-to-V5).

Regarding — ST-T wave Changes:

• As noted by Drs. Meyers and Smith — there is an interesting Brugada-like morphology to the ST-T wave in leads V1 and V2 (convex down RED line in V1,V2 of ECG #1). There is not enough ST elevation to qualify this as a Brugada-1 pattern — but, the clinical significance of recognizing this pattern is that the slight ST elevation in these leads is more likely to reflect a Brugada “phenotype” rather than acute septal infarction.

(For more on assessment of Brugada ECG patterns — CLICK HERE for a link to my 29-minute video on the subject. If you click on SHOW MORE under the video on the YouTube page — you’ll see a linked Contents to all in the video).

• Back to ECG #1: As per Drs. Meyers and Smith — there is subtle-but-real ST elevation in multiple leads. That said — the almost horizontal elevated ST segments in the inferior leads look less acute than one might have expected. These elevated ST segments are associated with prominent inferior T waves — and, reciprocal (albeit shallow) T wave inversion in lead aVL.
• Similarly the subtle-but-real ST elevation in leads V3, V4 and V5 has a shape that looks less acute than one might have expected (gently upward concave, as suggested by curved BLUE lines in V3 and V4 of ECG #1).
• NOTE: The different shape of the slightly elevated ST segments in leads V1,V2 of ECG #1 (curved-down RED lines) — vs the upward concavity ST segments in leads V3-thru-V6 (curved-UP BLUE lines) — in my opinion, adds further support that these are 2 different processes (ie, Brugada-like phenotype for the ST-T waves in leads V1,V2— vs recent acute injury for the elevated ST segments in leads V3-thru-V6).

Clinical IMPRESSION: Before finding this patient’s baseline tracing — I would have been hard pressed to know how much of what I was seeing in ECG #1 might have been due to the prior MI that this patient had — vs what might have developed since the onset of chest pain 11 hours earlier. This is the CHALLENGE I put forth to you earlier! Realizing there is NO way to be certain — these were my thoughts:

• What we see in ECG #1 probably did not just happen. Although possible to develop new Q waves in as little as 1-2 hours after acute infarction — I thought the size and number of Q waves seen here + the fragmentation in lead V3 suggested that at least some of these Q waves were the result of this patient’s prior MI. I would have guessed from the prominent T waves and subtle ST elevation that this patient manifests in ECG #1 — that he had suffered an acute event at the onset of symptoms (ie, ~11 hours earlier).
• That said — because there is still ST elevation in ECG #1, with inferior T waves that look like they may still be hyperacute + ongoing chest pain — cardiac cath sooner-rather-than-later seems indicated to clarify the clinical picture.

At this point in time — Finding a Baseline Tracing on this patient ( = ECG #2) proved invaluable! My thoughts on comparing ECG #2 with ECG #1:

• I was wrong about my hunch that at least some of the Q waves in ECG #1 were old. Other than lead V1 — there are no Q waves at all in ECG #2! Instead, R wave progression in this earlier baseline tracing was normal — with development of a fairly tall R wave already by lead V3. This means that the extensive Q waves in ECG #1 (including the fragmentation in lead V3) are new since the baseline ECG #2 was done. We have to presume (until proven otherwise) that these ECG findings are new since the onset of symptoms 11 hours earlier.
• There is virtually no ST elevation in ECG #2. Overall, I don’t see much difference in T wave appearance between ECG #1 and ECG #2. This left me with uncertainty regarding how acute the subtle-but-real ST elevation now present in ECG #1 might be. Did it develop days or weeks earlier? — or, sometime after the onset of symptoms within the 11-hour period prior to presentation in the ED? That said — persistence of chest pain + the ECG changes that developed between ECGs #1 and 2 would be indication for acute cath to clarify the clinical picture.

Apparently — the new ST elevation that developed in ECG #1 (compared to the baseline ECG) was not recognized. Several hours later, when the 1st troponin came back elevated — ECG #3 was obtained.

• I see no significant change in ST-T wave appearance in the limb leads between ECG #1 and ECG #3 done several hours later.
• However – there has been marked change in ST-T wave appearance in the chest leads in ECG #3! Even accounting for slight change in QRS morphology and amplitude in the mid-chest leads (suggesting some variation in precordial lead placement) — there clearly is now straightening of the ST segment takeoff (slanted BLUE lines in ECG #3) with more ST elevation in leads V3 and V4.
• Beyond-the-Core: The Brugada-like morphology in lead V1 of ECG #3 looks the same as it did in ECG #1 (curved-down RED line). It is interesting that the shape of the elevated ST segment in lead V2 of ECG #3 now manifests a flattened (BLUE-RED line) morphology that is intermediate between the curved RED line in lead V1 — and the upward slanting BLUE line in lead V3. I suspect the reason for this is a “fusion” between the Brugada-like ST segment effect being exerted on lead V2 — with what is now acute ST straightening and elevation in leads V2, V3 and V4 from the actively evolving anterior STEMI.
• Putting It All Together — Despite the history of a prior MI (with PCI) — the baseline tracing ( = ECG #2) shows no evidence of prior infarction. From the information available — it’s impossible to know if a 2nd event occurred sometime after ECG #2 was done — but before the onset of symptoms associated with this admission. What can be said — is that regardless of whether this marks a 2nd or 3rd cardiac event, that there is definite ECG and troponin evidence of an acute STEMI that is actively evolving between the time that ECGs #1 and #3 were done.

Final Learning Point: Thoughtful review of serial tracings + clinical correlation may retrospectively facilitate deduction of the time sequence of events.

• Final "P.S" — If the only ECG we were shown was ECG #3 in Figure-1 — it would be difficult on the basis of this ECG alone to distinguish between prior MI + LV aneurysm — vs — extensive antero-infero MI + an acute evolving event.

Our THANKS to Drs. Meyers and Smith for this challenging case!