Friday, April 12, 2013

Pulmonary Edema, Hypertension, and ST Elevation 2 Days After Stenting for Inferior STEMI

A male in his 40's who had been discharged 6 hours prior after stenting of an inferoposterior STEMI had sudden severe SOB at home 2 hours prior to calling 911.  He had no chest pain.  Medications were aspirin, clopidogrel, metoprolol, and simvastatin.  He was in acute distress from pulmonary edema, with a BP of 180/110, pulse 110.  Here is his prehosptial ECG:
There are inferior Q-waves with ST elevation T-wave inversion.  There is reciprocal ST depression in aVL and I.  There is ST depression in V2 and V3, with biphasic T-waves (down-up).  The computer read is:  *****Acute MI*****

The protocol for prehospital activation in the EMS system that this patient presented to requires 2 elements:

1) Chest pain
2) A computer read of *****Acute MI*****

Only 1 of 2 was present, so there was no prehospital activation.

The patient was transported to the ED.  On arrival, he was hypoxic, with saturations of 92% on room air.  He was in distress, diaphoretic, with signficant work of breathing.  He had diffuse crackles on exam and B-lines on chest ultrasound, and chest x-ray also confirmed pulmonary edema.   Blood pressure was 215/124 and HR 115 (on metoprolol).   Here is his ED ECG:
There is sinus tachycardia.  There are Q-waves in inferior leads, with ST elevation in II, III, and aVF, and reciprocal ST depression in aVL.  There is also ST depression in V2 and V3, now with fully upright T-waves.  Is this acute STEMI?

Of course, papillary muscle rupture and mitral regurgitation should be on the differential here, as in this case, but it is not very likely when the BP is so high.

Is this an acute STEMI?  -- Unlikely!

The prehospital ECG is indeed alarming, and activating the cath lab is certainly not wrong.  The ED ECG is less alarming: acute STEMI generally has an upright T-wave, unless reperfused or reperfusing (analogous to Wellens'), if not through the infarct artery, then through collaterals.  Thus, the absence of an upright T-wave in the leads with ST elevation (or an upright T-wave in leads reciprocal to ST elevation, such as V2 and V3 here) is a strong indicator of an open artery.  In this case, the inferior T-waves are down, and the T-waves that are reciprocal to the posterior leads (recorded in anterior leads) are upright, which suggest reperfusion of both inferior and posterior walls. See this explanation of posterior reperfusion T-waves.

The presence of the Q-waves, and the history of previous MI, are also strong clues that re-occlusion of the infarct-related artery is not the etiology of the symptoms.  Furthermore, the patient has no chest pain (certainly many STEMI do not have chest pain, but it should always make you especially scrutinize the ECG and the clinical situation) and there was severe hypertension.  The hypertension alone is the likely etiology of the pulmonary edema.

So it would be wise to look at the pre-discharge ECG, which was available:
There are Q-waves and ST elevation on this pre-discharge (post-stent) ECG.  The amount of ST elevation and depression is slightly less than on the ECG above, but there is also no tachycardia, which tends to exaggerate ST deviation.

The patient was treated with bilevel positive end expiratory noninvasive ventilation, given 3 sublingual nitroglycerine and started on a nitro drip titrating quickly to 80 mcg/min.  There was immediate relief of dyspnea, and the BP fell to 138 systolic with a pulse of 95 and saturations of 96%.

Before activating the cath lab, it would be useful to obtain another ECG at this point in time, and it is likely to appear very similar to this last one above, in which case the entire clinical presentation could be attributed to to the hypertension/pulmonary edema vicious cycle.

The cath lab was activated.  At angiogram, there was no change in the coronary arteries.  All symptoms were due to a combination of hypertension and fluid overload, and then the vicious cycle of pulmonary edema and SOB causing catecholamine burst, then more HTN and more pulmonary edema, etc.

Inferior LV "aneurysm" morphology

Electrocardiographic "LV Aneurysm" morphology simply means "persistent ST elevation after previous MI."  Not all such ECGs represent anatomic aneurysms (on echo this is "diastolic dyskinesis"), but do generally represent an area of dense akinesis on echocardiogram.  (This patient's previous and repeat echo had dense inferoposterior wall akinesis.)  I have discussed anterior LV aneurysm morphology at length in previous posts (for example, this post), but have not discussed inferior "aneurysm" nearly as much.

First, to be called "aneurysm," the MI must be at least a couple weeks old, so this case does not strictly apply.  Nevertheless, persistent ST elevation immediately after reperfusion is a sign of poor microvascular reperfusion and associated with worse function and higher mortality (and is a more accurate predictor of all kinds of outcomes than is TIMI flow), and also is associated with later persistent ST elevation (but not always).  This patient had had rapid reperfusion of his STEMI 2 days prior (TIMI-3 flow); nevertheless, his troponins rose very high and he had a dense wall motion abnormality.  This is typical of patients whose ST elevation is persistent.

Whereas in anterior "aneurysm," there is virtually always a QS-wave (or only a vestigial r-wave left), in inferior "aneurysm", a QS-wave is relatively less common and a QR-wave is very common.  For this reason, distinguishing acute inferior STEMI from inferior "aneurysm" is significantly more difficult than for anterior "aneurysm."

Nevertheless, in both instances, there are well-formed Q-waves, which is not very common in acute inferior STEMI (though very common in subacute STEMI, which also requires reperfusion therapy).

The patient did very well, and this time was discharged on lisinopril in addition to other medications.


  1. What about mechanical complication post-MI? Were you worried about papillary muscle rupture? Or even iatrogenic coronary artery injury? It appears the cath lab was activated and there wasn't a mechanical complication, but would emergent echo be more appropriate if the EKG was less supportive of STEMI?
    Thanks for the website, very educational stuff!

  2. That is a great question. I will add that the LV function on bedside echo was moderately decreased and that that should definitely be on the differential!

  3. Great case Dr. Smith...
    Since many STEMI present without chest pain, do you know the rationale of requiring chest pain to activation of the cath lab?


    1. Yes, since I helped write the protocol. Even though many STEMI do not have chest pain, the chances of SOB vs. CP representing STEMI are far lower. So you are likely to get fewer false positives if you require chest pain. Then for other symptoms, when the patient gets to the ED, the doc and medic together can put the pieces together. On the other hand, if the ECG is unequivocal (no question about it), they can activate, but not based only on the computer algorithm.

  4. Dr. Smith, thank you for these very helful information.

    As I have read from your blog, there is a way to discriminate anterior LVA vs acute anterior MI (T wave amplitude/QRS amplitude ratio in V1-V4), but is there any similar formula that applies for inferior LVA? And if not, how can we discriminate it vs acute inferior MI on ECG?

    1. Good Question. Much more difficult and I do not have a formula, and this is because inferior LVA usually has a QR wave rather than a QS wave. Nevertheless, in inferior LVA the T-wave is not as large, wide and may be partly inverted, whereas STEMI has a larger and upright T-wave.


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