Acute Severe Pulmonary Edema: What is the Diagnosis?

Here is an interesting case just presented in a conference today.  Thanks to Dr. Simegn, Asinger, Davies, and Bart for their input.

A 69 yo previously healthy woman had very sudden severe dyspnea.  The husband at some point reported that they had been physically active that day, and that the patient had complained of some chest pain one week prior for which she did not take his advice to go to the ER.  She presented in pulmonary edema, hypoxic on high flow O2, and sats were above 90% on Noninvasive Ventilation.  BP was 130/70.  Cardiac physical exam was unremarkable except for very coarse breath sounds. ABG was 6.99/44/201/11 on BiPAP.  Here is her first ECG:

The rate is 143.  There are p-waves, but in lead II there are apparently 2 p-waves for every QRS.   Is it atrial flutter?  The second apparent p-wave comes immediately after the QRS and appears to simulate ST elevation (Atrial flutter can frequently mimic ST deviation).   
However, if you measure these with calipers, they are not exactly spaced, so it cannot be be atrial flutter. 
There are also inferior Q-waves with T-wave inversion.   (In fact, there is S1Q3T3).  There is precordial ST depression which could represent subendocardial ischemia from severe tachycardia, hypoxia, etc, or it could be due to inferior posterior STEMI.

What else will help you to confirm that this is not atrial flutter, but rather is sinus tachycardia?  This is also important because there are notches after the QRS in the limb leads which, if not atrial flutter waves, are ST segment deviation.  Is this patient having a STEMI?

The ST segment and QT interval are remarkably short and could easily deceive you into thinking that this is not ST elevation, but rather flutter waves.

Considerations include:
1. Lead V1.  In sinus rhythm, the latter part of the p-wave in V1 is always negative, as it represents the depolorization of the left atrium, which is depolarizing away from lead V1.  In atrial flutter, the p-wave in V1 is usually upright.  Here it looks like a normal p-wave.  Furthermore, you don't see an identical wave directly between the p-waves and given that the baseline is pretty steady, it should be there.
2. If flutter, the rate should remain constant in spite of supportive care.

Now that we have established that the rhythm is sinus.  

A right sided ECG was recorded 6 minutes later:

The rate is still exactly 143.  Are we sure it is sinus tachycardia?

A bedside echo showed hyperdynamic function and a large RV.  The chest X-ray showed pulmonary edema.  The patient's respiratory status deteriorated and she was intubated.

Step back: what caused sudden respiratory failure with pulmonary edema?
--Does acute inferior-posterior STEMI alone do this?  Not if the pump function is hyperdynamic.
--Does atrial flutter alone cause severe pulmonary edema in someone who was previously healthy?  No.  (However, if this is atrial flutter, it is wise to cardiovert and this can only help the situation.  This was not done.  It appears that the rhythm diagnosis of atrial flutter was not considered.  If it is sinus, cardioversion will not hurt.)
--Does massive pulmonary embolism cause pulmonary edema?  Rarely, if ever.

A CT pulmonary angiogram was negative.

What test is now indicated?  What is the likely diagnosis?

Another ECG was recorded:

Now the rate is down to 120 and it is clearly sinus.  The p-waves are identical to those in the first ECG.  So those, too, were sinus.  Which means the waves after the QRS were indeed ST elevation and depression. There is inferior T-wave inversion and the upright right precordial T-waves are indicative of reperfusion to the posterior wall as well.  There is an infero-posterior STEMI of unknown age.   

It appears that the Q-waves were well formed at the time of presentation.

--Do inferior Q-waves appear immediately after the onset of a STEMI?  No.  [However, anterior Q-waves (QR-waves) can be present in the first hour after onset of anterior STEMI)].  

--The inverted T-waves also argue against an acute and persistently occluded artery.

Therefore, this patient's MI was subacute.  

Now, what do you think the diagnosis is?

Posterior STEMI puts patients at risk of papillary muscle infarction and rupture. (The posterior leaflet is supplied by posterior branches off the RCA and is vulnerable, whereas the anterior leaflet has its blood supply from the LAD and circumflex) An infarct in the last several days or one week is consistent with acute papillary muscle rupture.  This patient's presentation is classic for acute severe mitral regurgitation.

1. Acute pulmonary edema

2. Hyperdynamic heart (very low afterload out towards the left atrium and pulmonary veins

3. Severe pulmonary edema without hypertension.

4. Evidence of subacute inferoposterior MI (most occur more than 24 hours from onset of MI)

5. Absence of murmur because in acute rupture, the left atrium is small and as the LV contracts, the pressure between the LV and LA rapidly equalize so that  there is no lengthy period of turbulence.

An echo with Doppler was the diagnostic study, and confirmed papillary muscle rupture.  She was given immediate afterload reduction with nitroprusside, and taken for an angiogram which showed 2-vessel disease and a 90% RCA (the culprit) with flow.  Balloon pump was placed and she was taken for immediate valve replacement and CABG and did well.

The initial troponin was 2.4 ng/ml (probably still elevated from the MI one week ago), but did rise to 19 ng/ml by the next morning.  After CABG, it rose to 50 ng/ml.