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.

Annotated

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.