An Ischemic ECG and Bedside Echo shows diffuse dysfunction but with Apical Sparing

An approximately 40 y.o. male was in jail when he reported dyspnea.  He was brought to a small local ED where a chest x-ray showed pulmonary infiltrates.  He was hypotensive and hypoxic, and a provisional diagnosis of sepsis from pneumonia was made.  He had CT pulmonary angiogram which was read as “no PE.”  His lactate was 4.6 mEq/L and WBC count 20,000.  He was given levofloxacin, then transferred to a tertiary care center.

Upon arrival, his vitals were HR 115, BP 87/53, RR 30, T 37.3, and O2 sat 91% on room air. 

Breathing was labored, tachypneic.  He had cool extremities. 

He had this chest X-ray:

There certainly are pulmonary infiltrates, but it looks more like pulmonary edema.

 There was no fever.

 His troponin I returned at 6.8 ng/mL, at which point this ECG was recorded: 

There is ST depression maximal in V3 and V4, and a large R/S ratio in V2 and V3.
There is a suggestion of ST elevation in aVL, with reciprocal ST depression in II, III, and aVF.

In a patient with chest pain, one might diagnose posterolateral infarction with probable OMI.  And you would say it is probably subacute MI given the presence of high R/S ratio, suggesting some degree of completion of the posterior infarct.

But this is not a chest pain patient, so it is more difficult to interpret.  He was given aspirin. 

An ED echo was recorded:

This shows good contraction ONLY of the apex.

Again, good contraction ONLY of the apex.

These are typical of “Reverse Takotsubo.”

Standard takotsubo has apical ballooning and the base of the heart has good contraction.  Reverse takotsubo has good contraction of the apex, but not of the base.

His condition deteriorated, his BP dropped to 66/50, and he was intubated.

Here is the post-intubation CXR:

This looks more like pulmonary edema than pneumonia

The patient went to the cath lab and coronaries were clean.

With poor coronary perfusion pressure, a balloon pump was inserted.

Echocardiogram showed:

Left ventricular ejection fraction of 27 %.
Decreased left ventricular systolic performance moderately severe to severe.
Stress induced cardiomyopathy (Non TakoTsubo/”Reverse TakoTsubo” with involvement of base and sparing of apex).

Troponin I peaked at 7.7 ng/mL.

The etiology appeared to be stress from drug withdrawal.  

By 5 days later, the EF was 48% and the patient recovered.

For more cases of takotsubo: http://hqmeded-ecg.blogspot.com/search/label/takotsubo

For more on Reverse Takotsubo:

Respiratory Failure and ST Depression: Is there Posterior STEMI?

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Comment by KEN GRAUER, MD (9/4/2018):
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Insightful case with a fortunate ending. I’ll limit my comments to the ECG — for which I’ll suggest an alternative interpretation.
  • I see diffuse ST depression, which although maximal in V3, V4 — is present (to at least some extent) in a total of 8 leads. Leads aVR and V1 show slight ST elevation; leads aVL and V2 show ST coving. It is reassuring that pulmonary CT angiogram ruled out acute PE. In view of this, I interpreted this tracing as suggestive of diffuse subendocardial ischemia. Before reading what happened — I thought these ECG findings might reflect either severe underlying coronary disease – OR – the patient’s overall critical clinical condition.
  • There is an unusual Qr pattern with ST elevation in lead V1. This Qr pattern is really not consistent with incomplete RBBB, because there are no terminal s waves in any lateral leads. I’ve seen this pattern with acute PE, which pulmonary CT ruled out in this case. Then, there is very early transition, with a tiny but almost all positive QRS complex in V2, and a large predominantly positive QRS complex in V3. In retrospect (ie, knowing this patient had “reverse Takosubo” + diffuse pulmonary edema) — I suspect these cardiothoracic entities may account for this unusual sequence of R wave progression. I’d LOVE to see both a prior tracing on this patient, as well as a pre-discharge ECG after recovery of LV function — to see if this unusual precordial lead QRS pattern was new, and whether it normalized after the patient got better.
  • I thought the ECG in this case was less likely to represent posterior (or posterolateral) infarction with OMI — because leads leads V1 and V2 lacked the characteristic pattern of ST depression that I’m used to seeing with with acute posterior infarction. PEARL: In my experience, I’ve found Takotsubo cardiomyopathy as a common cause of a clearly abnormal ECG for which I could not logically explain all findings on the basis of a suspected “culprit” artery or other common pathology. Clinically, a cryptic combination of ECG findings as we see here should prompt consideration of Takotsubo even before we see the Echo. 

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