Saturday, January 20, 2018

A middle-aged man with severe syncope, diffuse weakness

A middle-aged male diabetic who is otherwise healthy was found unconscious by his wife, with incontinence.  He quickly awoke but was too weak to stand.  Initial vitals by EMS were BP 100/50 with pulse of 80 and normal glucose.  He remained weak and somnolent, and without focal neurologic abnormality.  He recovered full consciousness, but still felt weak and "not normal."  

There was a prehospital ECG:
What do you think?

He arrived in the ED and had this ECG recorded:
This one was sent to me for my opinion.  
I looked at it without any clinical information.
What do you think?

I wrote back that this is diagnostic of hypokalemia.  

It turned out the K was 2.6 mEq/L.

Why did I say this?

There is scooped ST depression in multiple leads, very typical of hypokalemia: I, II, aVL, V4-V6.

There are large U-waves.  Look particularly in V1 and V2.  This results in the appearance of down-up T-wave in V2; however, if it is a T-wave, resulting QT interval would be impossibly long.  Thus, it is a large U-wave, and the apparent QT interval is a QU interval.  Look directly above at V1 and you can see the U-wave clearly.

Such downsloping ST depression in V2 may frequently be misinterpreted as posterior STEMI (reciprocal to ST elevation of the posterior wall).

Case continued:

The patient had no chest pain or SOB.  His initial lactate returned at 5.0 mEq/L.  The patient and the vital signs completely recovered.  He seemed completely well.

After the K returned at 2.6, it was replaced.

The initial troponin I was 0.096 ng/mL, then rose to 0.191 at 2 hours after the first, and a second ECG was recorded 220 minutes after the first:
ST depression has resolved.
K has been replaced.

The third troponin I returned at 4 hours at 3.002 ng/mL, at which time the K was normal and another ECG was recorded that is not changed from the 220 minute one.

A 4th troponin returned at 6 hours at 7.905 ng/mL.

The clinicians decided to get a CT of the chest/abdomen/pelvis (I am not certain what they were looking for).  One image of the heart is shown here:
The arrows point to the inferior subendocardium.  It is dark because there is low contrast enhancement, which indicates absence of blood flow. 
This is a picture of inferior subendocardial ischemia.
Here is a closer up axial (transverse) view of the heart:
The arrows point to a subendocardial region with poor contrast enhancement due to ischemia.
This is posterior subendocardial ischemia.

This finding was seen in real time, and the patient was started on treatment for NSTEMI.

A repeat ECG was unchanged, and the potassium returned normalThus, in the presence of a normalized K, the ECG normalized in spite of ongoing myocardial ischemia.

A formal echo was done, which showed:
Normal EF
Regional wall motion abnormality (RWMA) of the apex, with dyskinesis (aneurysm)
RWMA of the distal inferior wall
Concentric LVH

A coronary angiogram was done a few hours later:
Culprit Lesion: 99% stenosis of the mid Circumflex with TIMI 1-2 flow (obstructed)
This was thrombus, acute (not a chronic lesion)
Diffuse severe disease of the mid and distal LAD
Chronic total occlusion of the mid right posterior descending artery (off the RCA) with left to right collateral filling 

Three vessel coronary artery disease with probable mid circ culprit for NSTEMI.  Successful circumflex PCI with excellent angiographic result, 0% residual.

If the source of collateral filling from the "left" was the circumflex, then the PCI of the circ would have restored this flow and resulted in full reperfusion to the inferior wall in addition to the posterior wall.

Here is a post PCI ECG:
Normal ST elevation in V2, not ST depression
Normal U-waves
Also: Now there is a large T-wave in V2 (posterior reperfusion T-wave) and inverted T-waves in inferior leads II, III, aVF (inferior reperfusion).
This is good evidence for reperfusion of the inferior and posterior walls.

So what happened?

There were several clinicians who thought the the ST depression was due to posterior STEMI.  It is possible but I think unlikely.
1. We do not have any evidence that there ever was full STEMI of the posterior wall.  The CT scan only shows subendocardial ischemia, which would not present with ST depression in lead V2.
2. The ECG looks to me like hypokalemia, and the K was 2.6 mEq/L.
3. The artery was open with flow at angiogram, corresponding to the subendocardial ischemia (not to transmural ischemia, which would lead to STEMI on the ECG) --though it is possible that the artery was fully occluded at the time of the first 2 ECGs.
4. There never was any chest pain or SOB or other anginal equivalent (and this was not a very elderly or debilitated person who might only feel "weak" with his MI, though he is diabetic).
5. The ECG normalized with a normal potassium while the myocardial ischemia was ongoing.

Initially when I heard about the case, I knew only these 4 things:
1. I saw the ECG, thought it was diagnostic of hypokalemia and confirmed it by the K of 2.6
2. I knew the troponins were elevated
3. I had heard only this about the angiogram: that there was a 99% circumflex lesion.

With this information, I surmised that the syncope was due to ventricular tachycardia from hypokalemia and the elevated troponins were from demand ischemia (type II MI) due to hypotension (because of VT) and poor flow through an extremely narrow chronic circumflex stenosis.

However, this was erroneous, as it turned out that the circumflex lesion was definitely due to acute thrombus (ACS), not a chronic lesion (as existed in the RCA).

Thus, one can only say that there were 2 pathologies at once:

1. Acute coronary syndrome of the circumflex with acute myocardial ischemia, that manifested without any chest pain or SOB, and that probably was not manifesting on the ECG.  [Although the scooped ST depression could have been a manifestation of diffuse subendocardial ischemia, all of it resolved with replenishment of the K in spite of the fact that the myocardial ischemia was ongoing.]

2. Hypokalemia, that did manifest on the ECG.

Ventricular Tachycardia?

Hypokalemia in the presence of myocardial ischemia is a very strong risk factor for acute ventricular dysrhythmia, so it is very likely that the syncope was due to ventricular tachycardia (VT).

Here are down-up T-waves of posterior MI: 

Series of Prehospital ECGs Showing Reperfusion

Here is down-up "T-waves" of hypokalemia: 

Biphasic T-waves in a Middle-Aged Male with Vomiting

Wednesday, January 17, 2018

I was texted this ECG: "Middle-aged male with Prehospital Cath Lab Activation"

A physician caring for his new arrival, a 50-something with acute chest pain and dyspnea and syncope, texted me this initial ED ED ECG. 

The computer read was "Marked ST Elevation, ***Acute MI***" 

No previous ECG was available.
What do you think?
Computerized QTc = 399 ms

My response was: "Normal variant"

Question: "De-activate cath lab?"

Answer: "It does not look like myocardial infarction".

He sent the prehospital ECG.  This also was read by the computer as "***Acute MI*** and was the basis for the prehospital activation.

Here it is:
My response: "Normal Variant"

I added: "One must always remember that there can be a coronary occlusion in the presence of a normal ECG.  So I cannot tell you that this patient does not have a coronary occlusion, but I can say that it does not show on the ECG."

He de-activated the cath lab.

The patient ruled out for MI by 4 serial troponins below the level of detection.

Let's look at the ED ECG more closely:
Sinus rhythm
There is ST Elevation in anterior leads: V2-V6
There is ST elevation in I, II, aVL

Why is this not STEMI?

First, I prefer to use my formulas and expertise to recognize coronary occlusion when it was not previously diagnosed or suspected.  I am reluctant to reverse a diagnosis of ***STEMI*** because I would rather there be a false positive cath lab activation than a false negative.

However, with some practice and expertise, this can be done with very high accuracy.

First, let's address the precordial STE:
1. The T-waves are not tall: the T/ST ratio is low (T-wave not much taller than ST segment)
2. High R-wave voltage (the single best predictor of whether subtle precordial STE is due to LAD occlusion or not!)
3. Very well-formed J-waves in V4-V6

You could consider using the formulas for differentiation of subtle LAD occlusion from normal variant STE.

One problem with this: there is a non-concave ST Segment in lead V2.  This is rarely seen in early repolarization (normal variant), and such cases were excluded from our study.  However, in this case, I happen to know from simple expert recognition that this ECG is an exception to the rule.

Using QTc = 399
RAV4        = 19
QRSV2     = 23
STE60V3  = 2.5

3 variable = 20.34 (very low, most accurate cutoff is 23.4)
4 variable = 14.84 (very low, most accurate cutoff is 18.2)

Second, let's address the limb lead STE

Inferior MI?  No
1. The inferior STE is limited to lead II, and has significant PR depression
2. There is no reciprocal ST depression in aVL, which is present in 99% of inferior MI.

High lateral MI?  No
1. The STE in I and aVL are associated with flat T-waves
2. There are well formed J-waves
3. There is no reciprocal ST depression in lead III.

ECG Diagnosis:

Normal variant ST Elevation vs. Pericarditis.  No evidence of MI (which is different than saying that the patient does not have MI)

Final Diagnosis:

No MI.  Uncertain whether there is pericarditis or normal variant. 

I favor normal variant for several reasons
1. No active chest pain
2. No objective signs of pericarditis (no rub, no effusion, no positional pain)
3. Normal variant is far more common
4. It simply looks to me like normal variant
5.  I believe that in this age of highly sensitive troponins that any ST elevation caused by pericarditis should be associated with some release of troponin.  Here all were below the level of detection.

Sunday, January 14, 2018

24 minute lecture: The False STEMI Non-STEMI Dichotomy from SMACC-Chicago: now online again

This is a lecture I gave it at Social Media and Critical Care Conference in Chicago (SMACC-Chicago) in June 2015.

It's title for the conference was "Myocardial Infarctions you must not miss!"

This Lecture is more aptly entitled: The False STEMI Non-STEMI Dichotomy.

The lecture had been offline for a while, but is back up!!

There is a lot of new data that further supports the ideas in this lecture, which is now almost 3 years old, but it is still very worth watching.

Sorry for the body movement: I just can't stand still!

The False STEMI Non-STEMI Dichotomy.

Myocardial Infarctions You Must Not Miss! - Steve Smith from Social Media and Critical Care on Vimeo.

Friday, January 12, 2018

Lecture, updated: Subtle ECG Findings of LAD Occlusion

This was recorded at a lecture I gave at Controversies and Consensus in Emergency Medicine in Northamptom MA.

This newly posted lecture is more up to date than this one which has been up for a while: 
One hour lecture on Subtle ECG Findings of Coronary Occlusion.  However, it is not quite as nicely produced.

As you watch this, remember that these are not missed STEMIs, rather these are missed opportunities to save myocardium!!

Thursday, January 11, 2018

Incredible case of evolution of terminal QRS distortion, then resolution after thrombolytics

For more on Terminal QRS distortion, see these posts:

Best Explanation of Terminal QRS Distortion in Diagnosis of Electrocardiographically Subtle LAD Occlusion

The paramedic crew of Rick Morton and Kim Baker, of Ambulance Victoria in Australia, took care of this patient.  Their friend Shane Chapman sent the case to me.  He asked some questions which I put and answer at the bottom.


A 60 something year old gentleman presented with chest pain radiating into left arm and a recent hx of SOB on exertion and fatigue for past 2 days.

Here are the ECGs and the times of their recording:
This shows very high ST Elevation. 
There are well formed S-waves in V2 and V3.  The S-wave in V4 is beginning to disappear.

At 1544, the S-wave in V3 is much small, has almost disappeared.
The S-wave in V4 has completely disappeared.
A Q-wave is developing in V3

Prehospital Thrombolytics were appropriately given at 1600.
Good work, guys!!!
At 1620, the S-wave in V3 is almost completely gone.

More ECGs were recorded:

At 1655, there is even less S-wave in V3
Note: this never quite meets the criteria for terminal QRS distortion (TQRSD), which is zero S-wave or J-wave in either of V2 or V3.
These criteria have importance in our study of 171 cases of normal variant ST elevation (early repolarization), not one case had TQRSD by this definition.

Terminal QRS distortion is present in anterior myocardial infarction but absent in early repolarization


At 1656, there is now Left Bundle Branch Block
The heart rate has increased, so it is unclear if this change is due to rate dependent LBBB, or if it is due to ischemia of the left bundle branch.
There appear to be hyperacute T-waves in II, III, and aVF.  Is there also an inferior MI (wraparound LAD to inferior wall? --this was one question they asked.)

Notice we can't calculate the modified Sgarbossa ratio because the S-wave is cut off.

LBBB is resolved
Notice that the ST elevation is receding (but rate is a bit slower)
Notice that the S-waves are re-constituting

Some persistent ST elevation, and persistent Q-wave in V3 and V4.
Successful reperfusion by thrombolytic therapy.

Now pain free, this ECG was recorded on arrival to the ED:
All ST Elevation is gone.  No Q-wave in V3 (these may indeed disappear with reperfusion)

Cath results:
Spontaneous coronary artery dissection (SCAD) of the mid LAD. 
No stent just managed medically and discharged home and doing well.

Could I please ask for your expert opinion?

Is this a wrap around STEMI?
        It has some features -- hyperacute T-waves appear to develop in II, III, aVF at 1656.
Can you explain the normal R-wave progression through the precordial leads? 
        This can be normal in anterior STEMI
Can you have normal R wave progression in the setting of STEMI?  

        Yes, you can.

Monday, January 8, 2018

High ST Elevation in a Patient with Acute Chest Pain

I was shown this ECG of a 50-something with acute chest pain:
What do you think?

I replied that this ST Elevation in precordial leads was normal variant STE.

Why did I say so?

1.  One can see that the QT interval is short (in fact, the computer measured it accurately at 285 ms.  With Bazett correction, that comes to a QTc of 381 ms (RR interval = 560 ms).  This computer has a proprietary algorithm (Veritas) that calculated a QTc of 349 ms.  In any case, this is a pretty short QTc for acute anterior STEMI.
2.  There are very prominent J-waves in V4 and V5.
3.  The R-wave amplitude is high.

3-variable formula: use 5.0 mm for STE60V3 = 21.94 (low value, indicating probably not STEMI)
4-variable formula:                                           = 17.0   (again, low value)

Go here for explanation of formulas:

12 Cases of Use of 3- and 4-variable formulas to differentiate normal STE from subtle LAD occlusion

There is also some fairly prominent PR segment depression in multiple leads, so pericarditis is possible.

V5 and V6 have a fairly high ST/T ratio, which favors pericarditis over early repol.

Further history: Patient presented with terrible pressure-like chest pain that woke him from sleep just prior to arrival. He had been having intermittent chest pain the last four days that he thought was his GERD. It resolved with acetaminophen but kept recurring. No reliable triggers. His pain at presentation was 10/10, mostly in his epigastrium, but radiating to his throat and back and worse when he is laying down or takes a deep breath.

There was an ECG from one month prior for comparison:
QTc 397
This also has normal variant STE, but not as much as above

31 minutes later another ECG was recorded:
QTc = 365
Now there is significantly less ST Elevation now

Due to profound ST Elevation that is dynamic and changed from previous, the cath lab was activated.


All coronaries were clean.

He was admitted and all troponins were below the level of detection.

The patient underwent a CT scan to rule out pulmonary embolism.

Here are the scan results:

1. Pneumomediastinum (almost certainly secondary to large perforation in
cervical esophagus) and findings concerning for extensive mediastinitis.
2. Small pericardial effusion.
3. Small right pleural effusion with overlying consolidation concerning
for infection or aspiration.
4. No evidence of pulmonary embolism

Diagnosis: esophageal perforation with mediastinitis and probable pericarditis (this does not necessarily mean the ECG represents pericarditis -- maybe and maybe not).


The ECG findings could be due to either dynamic early repolarization (normal variant ST elevation), or to pericarditis, or to a combination of the 2 entities.

Yes, normal variant ST elevation can be dynamic:

Increasing ST elevation. STEMI vs. dynamic early repolarization vs. pericarditis.

Alternatively, the ECG could represent pericarditis superimposed on early repol.  There certainly was pericarditis, but that does not mean the ECG findings were due to pericarditis.

This paradox is extremely well illustrated in this brilliant post

I do believe that in this age of very sensitive troponins (cTn) that pericarditis that results in ST Elevation will have at least detectable troponins.  We used to differentiate pericarditis from myocarditis using elevation of cTn.  There is no literature on this topic.  This article by my friend Pierre Taboulet is the closest I can find, but was published in 2000, many years before the age of highly sensitive troponins:

Serum cardiac troponin I and ST-segment elevation in patients with acute pericarditis

Friday, January 5, 2018

ST elevation in aVL with reciprocal ST depression in the inferior leads

Written by Pendell Meyers

A male in his 50s with history of thyroid cancer was brought to the Emergency Department after being found minimally unresponsive with sonorous respirations on his couch at home. Blood glucose level was 76 mg/dL. EMS administered naloxone, which was followed quickly by hyperventilation but no improvement in mental status. EMS performed RSI at that time using etomidate and succinylcholine, but intubation was unsuccessful. Luckily, BVM ventilation was easy in this patient, and he was bagged on the way to the ED, with oxygen saturation maintained in the mid-90s.

He was intubated immediately on arrival to the ED using ketamine and rocuronium. 

Here is the initial ED ECG:
What is your interpretation? 

What do you think about the ST elevation in aVL with reciprocal depression in the inferior leads???

The ECG is instantly diagnostic of hyperkalemia. There is likely sinus rhythm, with mildly widened QRS, peaked T-waves, and characteristic ST-segment morphology which slopes upward and begins to blend into the peaked T-wave (best seen in V4-V6). There is ST elevation in aVL, V1, and V2, with ST depression in V3-V6, and II, III, aVF.

As we have shown numerous times on this blog, hyperkalemia often may cause dramatic ST-segment deviations which may mimic STEMI (which is a poor surrogate for acute coronary occlusion).

See this case for an example

We have also shown cases where there has been simultaneous hyperkalemia and acute coronary occlusion, however in this case it would be appropriate to treat with calcium (and the other hyperkalemia treatments) to see if the ST elevation resolves. If the hyperkalemia on the ECG is resolved but the ST segment abnormalities remain, then one must reevaluate the situation and the repeat ECGs for acute coronary occlusion. Fortunately this patient did not present with chest pain or another presentation concerning for ACS, or else he could have been one of many other patients with hyperkalemia and ST segment changes who gets taken to the cath lab for possible acute coronary occlusion and suffers a delay in diagnosis and treatment of hyperkalemia.

Shortly after the ECG was performed, the treating physicians commented that the patient's heart rate began to drop, with further widening of the QRS on the monitor (no 12 lead ECG available). He was treated with calcium gluconate, followed by insulin and glucose, with immediate return to previous heart rate and QRS width.

Slightly decreased ST deviations throughout.

Initial labs included the following:
Na                 125 mEq/L
K                     8.0 mEq/L
Bicarbonate   13 mEq/L
BUN              90 mg/dL
Creatinine     10.24 mg/dL
Lactic acid      4.4 mg/dL
Troponin T     0.10 ng/mL
VBG pH         6.98
VBG PCO2    29 mm Hg

A dialysis catheter was placed for emergent dialysis. After several hours of treatment and dialysis, the repeat ECG is shown below:

All hyperkalemic findings resolved.

The patient did well.

Learning Points: 

You must be expert at recognizing hyperkalemia on ECG, and differentiating hyperkalemia from acute coronary occlusion.

Hyperkalemia may cause dramatic ST segment changes which may mimic acute coronary occlusion.

Tuesday, January 2, 2018

"This is not a Subtle ECG, right?"

A reader texted this ECG without any clinical information, with the question:

"This is not a Subtle ECG, right?"
My response:
"No!  Activate!"

The reader reported that this ECG was not recognized as abnormal and that he himself had found it at the doctor's station shortly after it was recorded.

The reader was concerned about the towering anterior T-waves and the small S-waves in V2 and V3.

The computer read it as benign early repolarization and the treating physician did not notice that it might be something else.

The reader activated the cath lab.

The reader asked another doc for whom he has great respect to look at it, and he also thought it was early repolarization.

It was a 40-something male with stuttering chest pain.

Outcome: proximal LAD occlusion.

The ST elevation does not meet STEMI criteria, as is very common in LAD occlusion.

However, to me and to my former resident, this is an obvious LAD occlusion because of the enormous T-waves, and the small QRS, with especially small S-waves, which almost meet the definition of terminal QRS distortion (but not quite).

I told him that V2 and V3 manifest a "forme fruste" of terminal QRS distortion, ("forme fruste:" an atypical or attenuated manifestation of a disease or syndrome).

This ECG is not obvious to everyone, as is clear from what happened in this ED.

And that is why I developed the formulas for differentiating the two entities.

How would the formulas fare?

[Here is an explanation of the formulas: 12 Cases of Use of 3- and 4-variable formulas to differentiate normal STE from subtle LAD occlusion]

I do not have the computerized QTc, but I measure the QT at 400 and the RR interval at 760.  So the QTc is 470.

STE60V3 = 2.5 mm
RAV4 = 9.5 mm
QRSV2 = 5 mm

3-variable formula: 30.7    (far greater than 23.4, the most accurate cutpoint)
4-variable formula: 23.8  (far greater than 18.2, the most accurate cutpoint)

Even if the QTc was only 400 ms, the values would still be positive:

3-variable: 23.49
4-variable: 20.154

Both of these values are extremely high and diagnostic of LAD occlusion.

Learning points:

1.  Use the formulas when there is ST elevation that you think is due to early repolarization.
2.  Be suspicious of coronary occlusion when the T-wave towers over the R-wave, especially if in more than consecutive lead.
3. Do not believe the computer when it says normal or early repolarization.  Interpret it yourself.
4.  Use the formulas when there is any question.

See many cases of occlusion in which the computer interpretation was totally normal:

A middle-aged woman with chest pain and a "normal" ECG in triage

Friday, December 29, 2017

Prehospital ECG looks very suspicious to the paramedic

This was sent by an anonymous paramedic.

"One of the paramedics at my work approached me the other day and asked for my opinion on two ECGs from a 50s male with sharp chest pain radiating to the back."

What do you think?

The medic asked for my opinion: "This is diagnostic of LAD occlusion, either mid or distal."

Paramedic thoughts: "I was concerned with the size of the T-waves in V4-V6 and of the STD in the inferior leads with slight STE in aVL."   

Smith comment: These T-waves in V4-V6 are all but diagnostic for being hyperacute.  When you combine this finding with the STE in I and aVL and the reciprocal ST depression in III, this is diagnostic of coronary occlusion.

See this post: 

Ten cases of hyperacute T-waves in V4-V6

Paramedic continues:  "Although your formula differentiating normal ST elevation from LAD occlusion should not be applied due to the ST Depression in leads II, III, and aVF, I decided to apply both formulas for the fun of it with the following values:" 

Note from Smith: the formulas really are intended to differentiate STE in V2-V4 that is normal from that which is due to occlusion.  This ECG does not have any appreciable STE in V2-V4.  The leads in question are V4-V6 and only because of T-waves, not ST elevation.

Paramedic continues

"For ECG 1: Computerized QTc: 394ms, STEV360ms: 0. R-wave V4: 4mm. QRSV2: 5mm. This received a positive 4-Variable value of 18.66." 
"For ECG 2: Computerized QTc: 404ms, STEV360ms: 0. R-wave V4: 2mm. QRSV2: 5mm. This received a negative 3-Var Value of 23.18, and a positive 4-Var Value of 19.72"

The medic recorded another ECG 21 minutes later:
No great change

Paramedic: "The ED that this patient was transported to almost never looks at pre-hospital ECGs unless transmitted prior to patient arrival (this one was not), so it is almost guaranteed that the findings would not be appreciated by the receiving physician."

"Anyway, after expressing the concerns that I had, the paramedic told me that the patient waited 90 minutes in the ED prior to being sent to the cath lab. (I did not ask, but I’m assuming that either troponin or serial ECG changes were responsible for the activation)."


"100% LAD occlusion stented. Patient is doing well. If I remember correctly, it was mid-LAD."

This comment is gratifying:

"On another note, I have been following this blog for just over a year now and I can say, without doubt, that i would have missed the subtle findings had it not been for your invaluable knowledge. For that, I sincerely thank you."

Wednesday, December 27, 2017

Ed Burns (from Life in the Fast Lane) sent me this one....

Ed Burns (who is the creator of the incredible, fantastic, Life in the Fast Lane ECG library) sent me this one....

This is a from a patient with chest pain:

What do you think?
There is very little ST elevation, only 1 mm at the J-point in V2 and V3

Ed's message was this:

Hi Steve,

A colleague sent me this ECG today.
I responded saying that it was a STEMI...
I thought the STs were a little too straight in V2-3 and the T waves a little tall, plus the reciprocal changes in lead III.

Can you improve on my assessment a little?
What is it that definitively makes the diagnosis of STEMI in this case?



Here was my response:

Good call!

There are several features:
First, as you said, there is a nearly straight ST segment.  It is very rare to have non-concavity (convex or straight) in any one of leads V2-V6 in normal variant ST elevation
Second, the QT appears slightly long for early repol.  Remember early repol is called early repol because repolarization comes early (relatively short QT)
Third, there is not enough R-wave amplitude in V4 for the T-wave size
Fourth, there is not enough QRS amplitude in V2 for that T-wave size.

The 3- and 4-variable formulas take the second, third, and fourth issues into account (see below):

Leads III and aVL are indeed somewhat suspicious; however, there really is no ST depression in III and a negative T-wave is normal, especially in the presence of a negative QRS (QRST angle is very small, less than 30 degrees)

Thanks for sending!


One more comment: I would not call it a STEMI, as this diagnosis is associated with ST Elevation "criteria" which this ECG does not meet.  One might call it:

1. Subtle STEMI

2. "Semi-STEMI"
3."Subtle occlusion" (in this case, subtle LAD occlusion)

Formulas use the following measurements
QTc =  (manually measured)                                                      = 400 ms  
ST Elevation at 60 ms after the J-point in lead V3 (STE60V3) = 2.5 mm
R-wave amplitude in V4 (RAV4)                                               = 9.5 mm
QRS amplitude in V2 (QRSV2)                                                 = 17 mm.

3-variable (STE60V3, RAV4 and QTc) = 23.48 (greater than 23.4 predicts LAD occlusion)
4-variable (adds QRSV2)                       =18.34 (greater than 18.2 predicts LAD occlusion)

These 2 cutoffs are the most accurate, not the most sensitive, nor the most specific.  

At 23.4, 3-variable formula had sens, spec, and acc of 86%, 91% and 88%

At 18.2, 4-variable formula had sens, spec, and acc of 89%, 95%, and 92%

The 4-variable is better for both but only in a derivation sample (needs validation!  Anyone??).

The patient did indeed have an LAD occlusion.

Final note on T-wave size: how do the formulas take T-wave size into account??   In our study, T-wave amplitude was not significantly greater for LAD occlusion vs. normal variant ST elevation (early repol also has large T-waves).  But large T-waves are only normal when there is high QRS voltage, as in normal variant.  ST elevation at 60 ms after the J-point is a measure of the slope of the ST segment; the higher the STE60V3, the steeper the slope. A steep slope correlates with a large T-wave and a flat slope with a smaller T-wave. 

Links to articles

3-variable formula:

4-variable formula:

Monday, December 25, 2017

See what happens when one fails to diagnose STEMI in LBBB and Paced Rhythm

Written by Meyers, edits by Smith:

A female in her 60s presented complaining of 2-3 days of fatigue and shortness of breath. She called EMS when her symptoms acutely worsened while she was shopping. EMS arrived and recorded a heart rate of 27.

On arrival to the ED she was noted to be in complete heart block. She was given atropine with transient increase in HR to 80s.

This ECG was recorded after response to atropine:
What do you think?


Sinus rhythm with 2nd degree type 1 (Wenckebach) AV block, best visualized in lead I.

Note: Wenckeback AV block occurs at the AV node (as opposed to the His bundle or below). Complete heart block that responds to atropine is also high (AV node, not His bundle or below). The AV node blood supply comes from a branch of the RCA.

On the other hand, 2nd degree type II and third degree (complete) block are likely to be due to LAD ischemia (in third degree block, especially if the escape is wide), and are unlikely to respond to atropine.

So the Wenckebach rhythm alone, and its response to atropine, can provide important information as to the etiology of the block.

How about the QRST?

LBBB is present with concordant ST elevation in leads III and aVF, with excessively discordant reciprocal ST depression in aVL. There is also concordant ST depression seen in the second QRS complex in V2. These findings meet both the original and modified Sgarbossa criteria, and are diagnostic of inferior and posterior wall acute coronary occlusion.

As a reminder or review for new readers, the modified Sgarbossa criteria are designed to identify acute coronary occlusion in the setting of LBBB, and are considered positive if any of the following three criteria are met in any lead when measuring ST elevation (at the J-point, relative to the PR interval):

1) Concordant ST elevation of 1mm or greater in any lead
2) Concordant ST depression of 1mm or greater in leads V1-V3
3) Excessively discordant ST elevation in any lead, such that the STE is 25% or greater of the preceding S-wave amplitude (20% was also still quite specific and even more sensitive)

There is a second rule which is less sensitive but very specific:
Any single lead with proportionally excessively discordant ST elevation or ST depression that is at least 30% of the previous S- or R-wave

See this post for further details on the modified Sgarbossa criteria.

The AV block is almost certainly attributable to the fact that the RCA almost always supplies the AV node.  Her prior recorded heart rate of 27 before atropine suggests she was in complete heart block at that time (no tracings available).

These findings were apparently not noticed in the setting of LBBB. A transvenous pacemaker was placed as the heart rate continued to drop.

What do you think?

Now there is a paced rhythm, as expected.  Do ST segments meet the modified Sgarbossa criteria?  In other words, are the ST segments either 1. concordant or 2. proportionally excessively discordant?  (See the third component of the first rule, or the second rule).

1. The STD ratio in lead I is indeed excessive by the second criteria (one lead with STE or STD greater than 30% of the preceding S- or R-wave).

2. Moreover, the first complex in lead III appears to 4.5 mm of ST Elevation with a 19 mm S-wave, for a ratio of 23.7% (almost 25%). The second complex appears to have a lower ratio (3mm/20mm = 15%).

3. The first complex in aVF seems to have 3mm STE / 14 mm S wave = 21%.

So the third criterion (excessively proportionally discordant STE at 25% of preceding S-wave) is almost met. Remember that, in the validation study, the rule using the third criterion at a 25% ratio was 99% specific and 84% sensitive, but a criterion of 20% was still 80% specific (and 94% sensitive) and thus is almost always due to occlusion.

So although the ischemia is much less visible in the paced rhythm, it is still diagnostic.

Look at lead V2: it is the transition lead in this case (where the QRS transitions from mostly negative to mostly positive), and the positive component of the QRS is slightly larger than the negative component. Thus, one expects ST depression in V2, and in order to indicate ischemia, it has to be proportionally excessive ST depression. Since the R-wave is 8 mm, and excessive STD is 30%, the ST depression would have to be at least 2.4 (2.5) mm to be ischemic. I don't believe it is.

This ECG by itself is be diagnostic of inferior and posterior acute coronary occlusion.

However, in this case, you get the benefit of seeing the ischemic findings both with and without pacing. For the vast majority of our chronic pacemaker patients, we don't get to see this, but they still deserve immediate diagnosis and treatment.

The initial troponin I was elevated at 0.44 ng/mL. After temporarily improving the heart rate with transvenous pacemaker, she was noted to be hemodynamically stable and to have "decreased shortness of breath but persistent fatigue." Coronary ischemia apparently was still not considered the most likely etiology at this time. Electrophysiology consult was placed, and together the physicians felt that the situation was more likely explained by acute renal failure and hyperkalemia (despite the fact that the highest potassium level measured was 5.9 mEq/L). Her second troponin I drawn 3 hours later was 0.38 ng/mL, which was interpreted as reassuring. She was admitted to the CCU and consented for a permanent pacemaker planned for the following morning.

Another ECG was recorded that night, with no mention of what symptoms prompted it:

This shows a huge amount of inferior ST elevation (ST/S ratio 1.0 or greater!) with reciprocal depression in aVL and I. This confirms ongoing transmural infarction of the inferior wall. The ST segment in V2 is inappropriately isoelectric (it should be elevated), suggesting ongoing posterior infarction.

Repeat troponin I around this time was rising at 0.68 ng/mL. Another troponin 4 hours later was 3.04 ng/mL. Unfortunately there is no available documentation about the thought process throughout the evening and night concerning the worsening ECGs and rising troponins. It seems that they scheduled her for cath the next morning.

Her last recorded troponin at 1:30am returned at 181.23 ng/mL!

At 7:45 am the next morning she went into asystole. She received CPR, atropine, epinephrine and was then noted to be in ventricular fibrillation. She was shocked once with return of spontaneous circulation, however her blood pressure continued to trend downward over the next 10 minutes. She was placed on dopamine and epinephrine drips, as well as receiving further hyperkalemia therapy (hyperkalemia had resolved on labs at this point). Another VF arrest was corrected with defibrillation. The patient remained critically hypotensive on multiple drips.

Finally the patient was taken to the cath lab where she was noted to have a completely occluded proximal RCA. Thrombectomy was performed with excellent angiographic result, however the patient continued to deteriorate despite balloon pump placement and continued pressors.

She expired on the cath lab table.

You may think this case is rare, that you and your colleagues would never miss ECG changes like the ones in this case, when the clinical scenario is so obvious. Yet I find these cases far too often. I cannot comment on the clinical decision making about NOT doing angiography when such patients have obvious clinical and ECG indications. What I can help with is helping clinicians to know what ECG findings to look for in the setting of LBBB and/or paced rhythms.

In one online quiz in Medscape, 50% of physicians believed the STEMI cannot be diagnosed in the presence of a paced rhythm.

The modified Sgarbossa criteria have been validated as the most accurate criteria currently available for identifying acute coronary occlusion in the setting of LBBB (but like all other criteria, are not perfect). We believe (based on cases like this and many others) that they are also applicable in paced rhythm, and are currently in the process of studying this. Preliminary results are positive, and the full multicenter results are on the way.

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