Tuesday, October 26, 2010

Tachycardia must make you doubt an ACS or STEMI diagnosis; put it all in clinical context

This 54 year old patient with a history of kidney transplant with poor transplant function had been vomiting all day when at 10 PM he developed severe substernal crushing chest pain. He presented to the Emergency Department with a blood pressure of 111/66 and a pulse of 117. He had this ECG recorded. He was rushed by residents into our critical care room with a diagnosis of STEMI, and they handed me this ECG:


There is sinus tachycardia with ST elevation in II, III, and aVF, as well as V4-V6. There is reciprocal ST depression in I and aVL. At first glance, it seems the patient is having a STEMI.
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But, remember, we do not evaluate and treat ECGs, we evaluate and treat patients. Even if this ECG is the first thing one sees (as it was for me), one should stop and think: "This is an unusual STEMI." Why?
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ACS and STEMI do not cause tachycardia unless there is cardiogenic shock. Are the lungs clear? Is the patient cool and pale? Then ACS (STEMI) might be primary; this might be cardiogenic shock.
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More often, tachycardia with ST segment abnormalities (elevation or depression) is due to an underlying illness (PE, sepsis, hemorrhage, dehydration, hypoxia, respiratory failure, etc.). One must clearly rule out these processes before jumping on the ACS diagnosis.
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Furthermore, notice the well-formed Q-waves in inferior leads. These must raise suspicion of old MI with persistent ST elevation.
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One very useful adjunct is ultrasound: bedside ED echo of his heart revealed no wall motion abnormality and hyperdynamic function. Large volume fluid resuscitation was undertaken. The K returned at 6.9 mEq/L. The HCO3 was 8. Cr was 13.4. Even after 3 liters of fluid, his CVP was very low.
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Troponins peaked at 0.275 ng/ml. An angiogram showed no acute coronary lesions. The patient was suffering from severe dehydration, possibly with sepsis.
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After stabilization, old EKGs and an old echocardiogram were found, demonstrating old inferior MI with persistent ST elevation (LV aneurysm morphology).

21 comments:

  1. I am surprised by the reciprocal ST depression, I was under the impression this would only be found in a STEMI. Was there ischemia due to the dehydration/sepsis, or are these electrical changes due to other reasons?

    Thanks.

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  2. ST depression is much more common in demand ischemia than is ST elevation, but ST elevation also occurs. If you do get ST elevation in inferior leads, and the ST axis is towards lead III, then there will necessarily be reciprocal ST depression in aVL because it takes the 150 degree opposite electrical "view". Make sense?

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    1. How do you determine the st axis?

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    2. Same way you determine QRS axis. It will be perpendicular to any isoelectric ST segment, and in the direction of the ST segment of highest voltage. It is a bit hard to explain in writing without demonstrating. If there is ST depression in I, II, V4-V6, and ST elevation in aVR, the ST elevation axis is towards aVR and diametrically opposite those leads with ST depression. In this latter case, the primary disorder would be subendocardial ischemia manifesting as ST depression in inferior/lateral leads, with reciprocal ST elevation in aVR. Think about it!

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  3. I should add: in this case, the ST changes were not even acute. But it demonstrates that even in old MI with persistent STE, there is reciprocal ST depression!

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  4. If I'm not terribly mistaken, the K level is at the cusp of STE and widening QRS (6.9-7ish). This pattern is also similar to that sometimes seen in DKA, which falls more in line with this patient's presenting vitals than I would -expect- to see in a STEMI.

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  5. I don't see any definite signs of the hyperkalemmia on the ECG. The QRS is normal (computer read it at 85 ms, and I think that's right. The PR is normal (180ms). You might say that the T-wave in lead III is peaked, but uncertain. In any case, the patient was immediately treated for hyperK because the level was so high. I suspect, with a Cr of 13 (baseline 2.6), that this was a very gradual increase in the K level, and thus the EKG findings (and corresponding danger of hyperK) were minimal.

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  6. Very intersting !! i think tacycardia can occur with STEMI even without signs of cardiogenic shock, consider the crushing sternal pain is very stressful to the patient and usually patients with MI are anxious which provoke tachycardia , am i right !!

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  7. I have a box of 355 consecutive LAD occlusions right next to me. The only ones with tachycardia had shock. There are now 3 studies proving that pain does NOT cause tachycardia. Anxiety does cause tachycardia, but these patients are usually calm (although with a look of doom) unless they are in shock (decreased brain perfusion).

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  8. Even when the rhythm is atrial fibrillation?

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  9. No, this does not apply to atrial fib. I should have specified that I mean sinus tach.

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  10. So if pain does not cause tachycardia and anxiety increases HR increasing 02 demand would it be more appropriate to consider Valium or Ativan over the traditional morphine?

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  11. Yes, that may help if anxiety is really the etiology of the tachycardia, which it only commonly is in intubated patients who are not adequately sedated; then lorazepam or propofol are useful.

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  12. does ST elevation caused by LV aneurysm make reciprocal ST depression??

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  13. Yes, just as it does in this case.

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  14. Shouldn't the old inferior MI have been visible on echo? Or is it possible to only have an "electric scar" with aneurysm morphology?

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  15. Ana, Good question. There should always be a wall motion abnormality, and, in fact, more than that: there will often be diastolic dyskinesis and there should always be at least wall thinning. It was not seen in this case probably because 1) bedside ultrasound was not done with the same quality imaging, machine, Definity contrast and 2) tachycardia makes it much harder to evaluate.

    Steve Smith

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  16. Great post even though it was some years ago..Some questions though:
    1) Does Q wave in lead III mean that it was a previous inferior MI? In other words, does Q wave ( like STE ) localize?

    2) If so, why did the Q wave localize to inferior leads instead of V1-V3 ( QS pattern ) if it was a LV aneurysm

    3) There are T wave inversions in lateral leads with ST depression in high lateral leads and with that ST elevation in inferior leads, could the aneurysm be localized anatomically in the inferior wall of the left ventricle?

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    Replies
    1. Ryan,
      1) yes, previous inferior MI, yes it does localize
      2) it is an inferior (not anterior) aneurysm
      3) Exactly. And inferior aneurysm does have reciprocal ST depression
      thanks,
      Steve

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  17. How about the upright T wave in inferior leads instead of inverted one? Shouldnt they be inverted if reperfusion occurs?

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    1. 1. In this case, we don't even know if there ever was reperfusion of the RCA.
      2. Reperfusion gives inverted T-waves during the peri-infarct period. Over time these become upright.

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