ST Depression and T-wave Inversions after ROSC from Resp and Cardiac Arrest after Head Trauma

This patient had a head injury and was unconscious.  He was found without respirations or pulse.  Prehospital CPR resulted in ROSC.  He remained comatose.

Here is his initial ED ECG:

What do you think?

There is sinus rhythm at a rate of about 75.  There is ST depression in right precordial leads, with deep T-wave inversions.  This is what catches the eye.

What SHOULD catch your eye?
















Whenever there is abnormal repolarization (abnormal ST segments and T-waves), the FIRST thing you should do it look for abnormal depolarization.

In fact, don't even get distracted by ST-T waves!  Even before you look at them, look at the QRS.

Is it normal?  Abnormal?  Is there an abnormal axis?  Abnormal voltage?  Abnormal R-wave progression in precordial leads?   Abnormal Q-waves?  RBBB?  LBBB?  Etc.

You should read the ECG systematically!

Look for:

Rhythm, rate
P waves
PR interval  
QRS Duration (IVCD? RBBB? LBBB? Paced?)
QRS Axis 
Voltage 
Abnormal Q waves
R-wave progression
J-waves
S-waves

Only then do you look at:

ST segments
T wave axis (inversion?)
Size of T-waves, whether upright or inverted
QT interval
U-waves.


Only THEN should you look at the ST-T.

But let's be realistic!!

Realistically, our eyes are drawn to the ST-T.  We can't help ourselves.

Therefore, we have to be aware that the ST-T is dependent on the QRS.

In this case, there is a deep S-wave in lead I.  There is right axis deviation.

Whenever there is a right axis, you should think about right ventricular hypertrophy.  (There is also large voltage consistent with LVH.)

How would you verify that??

Look at the R-wave in V1.  If is it abnormally large, you have RVH until proven otherwise.

So I looked for it and, lo and behold, there it is!  A large R-wave in V1.

Now it is useful to know that these ST-T morphologies are CLASSIC for RVH.

I knew immediately that all of this was due to chronic RVH with secondary ST-T abnormalities.  I was not concerned for ischemia at all.

In other words, all these findings were old and had nothing to do with the patient's present condition.

Later, it was confirmed from outside records that this patient has pulmonary hypertension from Eisenmenger's syndrome.



Comment

One might think that these are central nervous system T-waves, but they are not.  Here are some examples of CNS T-waves:

Bizarre T-wave Inversions in a Patient without Chest Pain

Here are Ken Grauer's comments:

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KEN GRAUER, MD Wrote the Following:

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GREAT case — with the most important point emphasized being the need for systematic ECG interpretation. We are not told the age of this patient … — but I’ll presume it is an adult. I would add the following points to those made by Dr. Smith:

• i) It does not matter which system you use for ECG interpretation — as long as you automatically apply YOUR system to the interpretation of EACH and every ECG that you see. Unless this is done religiously — it is all too easy to miss important findings (as many of you probably did for this ECG …); 
• ii) Being “systematic” does NOT slow you down. On the contrary, in addition to organizing your thinking and clarifying what you know for certain, and which ECG findings you might be uncertain about — with a little practice, being systematic will dramatically SPEED UP your interpretation — because you will no longer be going back-and-forth repeating your assessment of various findings; 
• iii) WHATEVER system you use — you must interpret intervals (PR/QRS/QT) early in the process — because if there is a conduction defect (ie, wide QRS) that you fail to recognize, the criteria for assessment of ALL parameters that follow will change; 
• iv) I favor a system that sequentially assesses 6 key parameters = Rate-Rhythm-Intervals (PR/QRS/QTc)-Axis-Chamber Enlargement-QRST Changes. 
• v) The purpose of the “R” in QRST Changes, is so that you do not overlook the finding of a dysproportionately tall R wave in lead V1, like we have here. Putting together the findings we have for this ECG — this >10mm tall R wave in lead V1, together with RAD (right axis deviation) and the anterior ST-T wave depression — suggests probable RVH and/or pulmonary hypertension. But this tracing does NOT suggest “pure” RVH — because there is also a surprisingly deep S wave in V1 (which is typically absent with pure RVH), as well as tremendously increased biphasic QRS amplitude (≥50mm) in V2,V3 and V4 ( = Katz-Wachtel phenomenon) — which strongly suggests LVH as well as RVH ( = biventricular hypertrophy).