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

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.

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.