Thursday, February 21, 2013

Extremely Subtle ECG, but Bedside Echo Shows Wall Motion Abnormality and Ischemic Pain Cannot Be Controlled Medically

A male in his 40's with no previous cardiac history had presented to a clinic recently with chest burning, had a nondiagnostic ECG, and was diagnosed with reflux. He presented to an ED with 2.5 hours of chest burning a few days later.  His BP was 152/84.  Here is the initial ECG:
Sinus rhythm,  Q-wave in III with minimal ST elevation and minimal ST depression in I and aVL.  There is a suspiciously minimally biphasic T-wave in V6.  This is a nonspecific ECG.

The ECG from the clinic was sought for comparison:
Compared to this one, the ST depression in I and aVL seen above is new and T-waves are nonspecifically different in diffuse leads. 

The patient continued to have chest pain of an ischemic quality. The clinical presentation worried the ED physicians, so they performed a bedside ultrasound (parasternal short axis view):

Cardiac Ultrasound Parasternal Short Axis from Stephen Smith on Vimeo.

The curved white line shows the wall (lateral) which has hypokinesis.  Note that the hypokinetic area is full thickness, not thinned out as in old MI.  Therefore, it is consistent with acute infarct.
The wall motion abnormality confirms that these nonspecific T-wave changes are indeed ischemic.  The chest pain is therefore ischemic.  The physicians attempted to control the pain with nitroglycerine, both sublingual and intravenous, titrating to 60 mcg/min, and BP down to 100/57.  Thus, they were trying to treat this "NonSTEMI" medically, as there was no ECG indication for immediate reperfusion therapy.

They recorded a posterior ECG:
Leads "V4" to "V6" are really V7 to V9.  Note the low voltage of posterior QRS because of more distance from the heart and because of air (lung) between heart and ECG leads.  Thus, only 0.5 mm in 1 lead is considered posterior  STEMI.  Here there is no ST elevation.  However, leads V2 and V3 are the same as the first ECG and the T-waves show are not very different.  Thus, the patient has dynamic T-waves.

The echo and dynamic T-waves confirm ACS.  Definite ischemic pain which is refractory to medical therapy is an indication for reperfusion therapy.  It is important to remember that approximately one third of NonSTEMI have an occluded infarct related artery at cath.

Heparin and Clopidogrel were given and the patient was taken to cath (after which the first troponin returned slightly elevated).  He was found to have severe LAD disease and an occluded 1st Obtuse Marginal off the circumflex.  This was opened and stented.  The troponin I (Ortho Clinical Diagnostics) peaked at 45.8 ng/ml (quite high).   Formal echo later showed anterolateral hypokinesis and an EF of 55%.

The artery was occluded and the myocardial territory at risk was very significant, yet the ECG did not have diagnostic ST elevation.  This is common.  Fantastic management led to rapid therapy and salvage of significant myocardium.


  1. is important to note that the RWMA involves a "thick" portion of myocardium, and therefore most likely to be new.

  2. Mr. Smith, what do you think about minimal but new ST elevation in leads II and aVF ?

  3. This is exactly the kind of case that makes me want to be a better cardiac sonographer.

    I'll be an ultrasound fellow next year. Do you have good recommendations for echo resources, online or in print?

    Keep up the excellent teaching! Thank you!

    1. has a lot of ultrasound resources. look around the site. It is run by my colleague Scott Joing and is where this blog is housed. It is fabulous.

  4. Dear Dr. Smith, I love your ECG example cases and I'm delighted by the scientific evidence that you cite.

    However, I'd love to know more about the specific cardiovascular risk profile of your cases, which (at least in our chest pain unit) contrbute a great deal to the decisions being made: Small ECG changes in a diabetic, hypertensive patient would be interpreted differently thatn in a young female without any risk factors.

    Cheers from Germany,

    1. Nick,
      You are so correct that the pretest probability of disease is extremely important when interpreting a test (i.e., the ECG). However, even with a very low pretest probability, there are some situations in which the test is so clearly positive that the post-test probability is very high in spite of a low pretest probability. A subtle ECG in someone with a low pretest probability is probably not MI, and you would be slower to take definitive action (activate the cath lab) without confirmatory evidence. In this case, the confirmatory evidence was the echo.
      Steve Smith

  5. Hi Steve

    Another great case. Just one point - although you state that the posterior leads V7-9 in the third ECG were V4-6 moved around, and therefore V1-3 are dynamic, I am suspicious that in fact the leads V1-3 were moved to V7-9 given that V1-3 in the third ECG are IDENTICAL to the leads V1-3 in the first ECG. Don't think it changes the overall message, but it leaped out at me a bit.

    1. Look more closely. In the third ECG, V1 and V2 have a significantly larger R/S ratio AND there is now a biphasic T-wave in V3. Also, the low R-wave amplitudes of V4-V6 prove that these are, in fact V7-V9.

  6. Correction to my last comment - I meant that V1-3 in the third ECG looks suspiciously like V4-6 in the first ECG...

    1. Now I see what you mean, but that implies that the tech moved all 6 leads over V1 to V4, V2 to V5, etc. Hard to imagine that would be done, but possible.

  7. Good case, Steve. The electrocardiographic distribution of changes don't seem to be consistent with an acute OM-1 Occlusion (ST-Depressions in I & AVL, Dynamic right precordial T's, etc) Any explanation?

    1. Sam,
      OM-1 supplies the posterior wall, and this could lead to dynamic T-waves in V2, V3.


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