Respiratory Failure and ST Depression: Is there Posterior STEMI?

The ultrasound in this case was recorded by Dr. Robert F. (Rob) Reardon, one of my partners here at Hennepin County Medical Center (HCMC) in Minneapolis, and one of the world leaders in emergency ultrasound.  He is also an editor of this great new textbook of emergency ultrasound (Ma, Mateer, Reardon, Joing, eds.), and one of the authors of the Cardiac Ultrasound chapter (other authors of this chapter are Dr. Andrew Laudenbach (also of HCMC) and Dr. Scott Joing (also of HCMC, and the creator of the outstanding FOAMed site, www.hqmeded.com).

Case

A middle-age woman with a history of emphysema presented in severe respiratory distress and respiratory failure.  She was intubated emergently in the ED.  Her venous blood gas after intubation had a pH of 7.16 and pCO2 of 66.  The Chest X-ray was suggestive of pneumonia, but not pulmonary edema.  The following ECG was recorded:

There is sinus tachycardia, and ST depression that is maximal in V3 and V4, suggestive of posterior STEMI, or possibly subendocardial ischemia.  [However, subendocardial ischemia is usually diffuse, and therefore has an ST depression vector towards the apex of the heart (towards V5 and V6.  That is to say, the maximal ST depression is usually in I, II, V5, and V6, with reciprocal ST elevation in aVR.]

A posterior ECG was recorded:

There is ST elevation in posterior leads V7 and V8.  

Although this meets criteria for posterior STEMI (0.5 mm in 2 leads), there will virtually always be some ST elevation in posterior leads when there is ST depression in anterior leads, as these are opposing leads. 

[There is an exception to this rule, and that would be in pericarditis, when there is an ST elevation vector that goes from endocardium to epicardium throughout the entire heart, with an ST elevation summation vector towards the apex.  In such a case, there is diffuse ST elevation, including towards the posterior wall.]

Thus, there is probably posterior transmural ischemia.  Is this ACS with posterior MI?  The presentation of respiratory failure without pulmonary edema is not at all typical for ACS.  The patient apparently has a COPD exacerbation with pneumonia.  She could have 2 pathologies at once, but this is less likely.

An ED cardiac echo was performed at the bedside:

This subcostal view shows poor contractility at the entire base of the heart, and excellent contractility at the apex.  There is no wall motion abnormality in a coronary distribution.

Dr. Reardon made a diagnosis.  What is it?












Reverse Takotsubo!  (See below for description of Takotsubo and Reverse Takotsubo)

Case continued:

The patient was admitted to the Medical ICU.  She recovered.  Her max troponin I was 2.2 ng/mL.  Formal Echo also showed Reverse Takotsubo, with EF of 35%.  Echo 2 months later showed full recovery of EF.

She returned in respiratory distress 5 months after the first presentation, and required intubation again.  Here is her ECG from that visit:

Very concerning for Anterior STEMI

A bedside echo showed what appeared to be an anterior wall motion abnormality.  Cardiology was immediately consulted for a formal echocardiogram.  It showed an EF of 15% with a circumferential loss of function at the mid-section, with preservation of the apex and the base.  (This is called mid-ventricular stress cardiomyopathy).

Again, the troponin I peaked at 2.2 ng/mL.

An angiogram was done and showed normal coronary arteries.

The LV function eventually recovered again.





Stress Cardiomyopathy, Takotsubo and Reverse Takotsubo, and Mid-Ventricular Takotsubo Cardiomyopathy

In Takostubo stress cardiomyopathy, caused by small vessel ischemia from high catecholamine influence, there is poor contractility at the apex, causing "apical ballooning," which has the appearance of a Japanese octopus trap, or "Takotsubo"  Here is a left ventriculogram of Takotsubo SCM.

Standard Takotsubo with Apical Ballooning.

See this case for ECG and Echo video of Takotsubo Stress Cardiomyopathy that Mimics STEMI.


Reverse and Mid-Ventricular Takotsubo Stress Cardiomyopathy (SCM):

Reverse Takotsubo SCM is the term used when the LV dysfunction is of the base, and not the of the apex.  Thus, there is no apical ballooning. As in standard Takotsubo, the dysfunction is circumferential, not in a vascular territory, and not due to ACS.  

Reverse SCM has been described in many stressful situations, just as standard Takotsubo SCM, including sympathomimetic drug abuse, energy drinks, serotonin syndrome, anaphylaxis, high dose epinephrine (adrenaline!), pheochromocytoma, subarachnoid hemorrhage, sepsis, and dobutamine stress.

Reverse Takotsubo may be more common in younger patients, but there is little systematic data on the condition.  One small registry of 103 SCM patients, 20 of whom had reverse Takotsubo, showed that the reverse type had higher incidence of triggering stress (100% vs. 77%), less dyspnea, pulmonary edema, and cardiogenic shock, and less T-wave inversion on ECG.

Mid-ventricular Takotsubo is the term for poor function of the mid LV (ballooning of the mid-LV), with good function of BOTH the base and the apex.  It is less common than either of the other forms.

Of course, if it is SCM that does not have apical ballooning, it does not look like an octopus trap, and therefore perhaps should not be called Takotsubo at all.

There is also a claim of a 4th type, "localized" SCM (with focal wall motion abnormalities mimicking ACS).  The claim is substantiated only by case reports, such as this one, which cannot establish with certainty the absence of a thrombotic coronary lesion.

Take Home Lesson:

When the clinical situation is stress (such as respiratory failure from COPD in this case -- not from pulmonary edema), and the echocardiogram shows circumferential dysfunction, whether at the base, mid-LV, or apex, then stress cardiomyopathy is very likely the etiology of the ECG abnormalities.