Syncope and Flash Pulmonary Edema with T-wave Inversions in V1-V3

A 60 yo with no cardiopulmonary history, felt dizzy, cold and clammy, and then had syncope.  She denied SOB or Chest pain.  Pulse oximetry was 95%.  Lung and heart exams were normal.

A bedside echo done by an ultrasound-fellowship-trained EP was recorded as normal.

She had an ECG as part of her syncope workup:

There is an abnormal Q-wave in lead III (greater than 40 ms in width is abnormal).  There is nonspecific T-wave flattening in in inferior leads and in V2 and V3, and nonspecific T-wave inversion in V4-V6.

With the abnormal, but nondiagnostic, ECG, a wider workup was initiated.

A troponin I returned elevated at 0.290 ng/mL (normal, less than 0.030).

A chest X-ray was obtained:

This shows pulmonary edema.

So we have:
Syncope, mild flash pulmonary edema, and an elevated troponin with a nondiagnostic ECG.

A repeat ECG was obtained:

Now there are developing T-wave inversions in V1-V3 and also lead III.

This pattern is classic for pulmonary embolism.  Click on this link for a detailed post on the ECG in pulmonary embolism.

However, pulmonary edema is very rare in pulmonary embolism.  PE decreases pulmonary artery wedge pressure (an increase is what leads to cardiogenic pulmonary edema).  For this reason, it was assumed that the T-wave inversions are more likely due to LAD ischemia (Developing Wellens' waves), and not due to PE.  This is spite of the fact that the T-wave inversions are atypical for Wellens' waves: pattern A has slight ST elevation with upward sloping ST segment, then sudden downward drop; pattern B has deep symmetric T-waves.

See this photo of Figure 1 in Wellens' first paper
(de Zwann C et al.  Am Heart J 1982; 103(4 part 2):730-6:

Classic Wellens' Pattern A and Pattern B Waves.

For some unknown reason, the nomenclature was widely misrepresented across emergency medicine publications: Pattern A has been referred to as Type 2, and Pattern B as type 1 (!!!!)

The patient was started on heparin and Plavix (and aspirin, of course) for presumed anginal equivalent (this could not be called Wellens' syndrome even in T-waves were typical, because the syndrome requires an episode of resolved chest pain. This patient had no chest pain.

A repeat troponin returned at 0.438 ng/mL, and an NT-proBNP returned elevated at 1800 pg/mL (normal less than 900).

She was admitted to the hospital.  Serial troponins declined.

Echocardiogram:

A formal echo showed an EF of 50%, probable inferior wall motion abnormality (consistent with Q-wave in lead III), concentric LVH, and normal pulmonary artery pressure.   Right ventricular enlargement with probably reduced function.

She then underwent a CT coronary angiogram:

Coronary arteries: all normal, with calcium score of zero
However, also seen: Bilateral pulmonary embolus seen in the bifurcation of the left
pulmonary artery extending down into the descending branches and in the
lingular branch. Clot seen in the main right pulmonary artery, in the
upper lobe branch, middle and lower lobe branches that is nonocclusive.

Bilateral Pulmonary Trunk Thrombi

This shows some probable pulmonary infarction and may be what we see on chest x-ray that appears to be pulmonary edema.

Comment: 

PE rarely has pulmonary edema.  A search of the literature showed few case reports, all very old.

One does not typically scan everyone with apparent pulmonary edema.  Had the patient undergone standard angiography, the diagnosis of PE would only be considered because of absence of coronary disease.  And such absence may or may not lead one to pursue other diagnoses.

Remember that Pulmonary Embolus:

1. Causes anterior T-wave inversion plus T-wave inversion in III
2. Often has elevated troponin
3. Often has elevated BNP
4. May mimic ACS


Lesson: 

1. What appears to be pulmonary edema on chest X-ray may, in fact, be infarct or infiltrate. 
2. The ECG was more accurate in this case than other diagnostic modalities, and could have directed the diagnosis in the right direction.

Great Question:

Assuming I understand the classification system, this is submassive PE. What is your view about thrombolytics in a case like this?

Great Question.
At the time of syncope, it was probably massive PE.  By the time she was in the ED, it was no longer massive or submassive, as she had no symptoms, no tachycardia, and normal Echo.  Just like coronary occlusion, pulm artery occlusion can be transient, and the patient recovers.  The treatment should be based on the physiology at the present moment. The elevated biomarkers are due to the severe insult that happened prehospital, but are clearly not ongoing.  And clot burden does not correlate with outcome, hemodynamic compromise, or lack thereof, is what we base therapy on.

So: no thrombolytics even if one is predisposed to give them in submassive PE.