Sunday, May 17, 2015

ST elevation and depression: is it ischemia? The entire clinical context is critical.

This patient has a history of cardiomyopathy (EF 10%) and IVCD and heart failure and presented with altered mental status.   BP was 87/52, pulse 90, saturations 100%, and respirations 14.   An ECG was recorded:
There is sinus rhythm.  The P-wave in V1 has a huge negative component, diagnostic of left atrial enlargement.  The PR interval is 360 ms (the computer read it as 227 ms).  The QRS = 134 ms, so it is an IVCD (intraventricular conduction delay), but is not LBBB because of Q-waves in I and aVL.

There is a large amount of ST elevation in V3-V5, and ST depression in V6.  But there are also very deep S-waves in V3-V5 and a very tall R-wave in V6.  The highest ST/S ratio is about 10% (normal).  

There was an ECG from 4 months prior:
Atrial fib.  QRS = 118 ms.  Voltage was high then too, but ST segments were not.  So the ST elevation is new.

The physicians were worried about this and showed it to me.

I said that this is very unlikely to be ischemia because of:

1) the severe cardiomyopathy
2) the high voltage
3) relative clinical stability in a patient with a baseline EF of 10%
4) presentation without chest pain

I recommended a bedside echo and further eval. This was done and showed very poor LVF and no WMA.

Electrolytes and Venous Gas results returned:

Na = 117 mEq/L
K = 2.7 mEq/L
Chloride = 68 mEq/L  (this indicates metabolic alkalosis)
CO2 = 46 mEq/L
Anion Gap = 3 mEq/L (so there is no serious metabolic acidosis)
Venous pH = 7.58 (normal = 7.33), corresponds to an arterial pH of 7.65 (very alkalemic)
HCO3 = 45
Venous pCO2 = 47 (normal = 47), which corresponds to an arterial pCO2 of about 40 mmHg.

This actually represents a superimposed respiratory alkalosis: when the HCO3 = 45, the patient should compensate with a decrease in minute ventilation, such that the arterial pCO2 should be about 57 (0.9 x HCO3 + 15), and venous pCO2 should be slightly higher, around 62-64 mmHg, not 47 mmHg.

For a comprehensive presentation on Acid Base disturbances, see my 55 minute lecture on the topic.

So the patient has profound metabolic disturbances [hypokalemic metabolic alkalosis without any respiratory compensation (and thus a superimposed resp alkalosis)], and this explains the ECG findings.  After some treatment, this ECG was recorded 23 hours after the first:
It is normalizing

At 36 hours, after more electrolyte correction:
Looking more and more like the old ECG

At 3.5 days, there was some tachycardia:
This was diagnosed as SVT, but it is, in reality, sinus tachycardia.  See image below with arrows.

Arrows point to P-waves. Note the P-wave morphology, and PR interval, are the same as in the slower sinus rhythms.

Learning Points:

Cardiomyopathy, especially with metabolic derangement, can result in profound PseudoSTEMI patterns.


  1. Stephen...

    Thanks so very much for making your excellent book available to all in pdf format. I especially appreciate the synopses for each reference at the end of the chapters and the case presentations and comments. I do have one question, however. On page 17 it states that Leads V1 and V2 should be placed in the third ICS instead of the fourth. I cannot find any other references recommending that. Is there a particular reason for placing V1 and V2 in that interspace or is it a mistake?

    Jerry Jones MD FACEP

    1. Jerry,
      Thanks. This is a mistake in the book. So sorry!
      Steve Smith

  2. Thanks a lot for the interesting case.
    Do severe metabolic derangements always cause ECG changes? Are there any particular patterns?

    1. Not always and it depends on the metabolic derangement. A big topic that can't be adequatly covered in this response, but search in this blog for hyperkalemia, acidosis, hypokalemia, hypercalcemia, hypocalcemia, etc. and you'll find a lot of useful information.
      Steve Smith


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