Saturday, February 14, 2009

Hyperacute T waves

Below are several examples of hyperacute T waves.

Click here for more great examples of hyperacute T-waves.

Click here for cases of "inferior" hyperacute T-waves.

Case 1 (Hyperacute T waves with ST depression--LAD occlusion).

The following is a perfect example of Anterior MI with LAD occlusion but WITHOUT any ST elevation. This is seen commonly, but only recently reported on by de Winter, Verouden, Wilde, and Wellens' in a long letter to the New England Journal (NEJM 359(19):2071-2073; Nov. 6, 2008).

The authors reported this morphology in 2% of LAD occlusions. The morphology is as follows: 1-3 mm of upsloping ST depression in leads V1 to V6 that continues into tall, positive symmetrical T waves, with normal QRS and loss of R-wave progression and with 1-2 mm ST elevation in aVR. Interestingly, they found that this was not a transient feature that later progressed to ST elevation, but that it remained static until angiography up to 50 minutes after the initial ECG. The mean time from symptom onset was 90 minutes. K levels were normal. MI was very large as measured by high CK-MB.

Case 2 (Hyperacute T waves present AFTER ST elevation is resolving).  Click here for an even better case of this phenomenon.

This is the EKG of a previously healthy 40 year old man with one hour of chest pain and profound weakness and sense of "doom". He has a history of HTN, smoking, and family history. Vital signs and exam were normal.

This ECG show large symmetric T waves, best distinguished from those of early repolarization by the absence of large R-waves (in this case, the R-wave amplitude is very small). It also helps that there is inferior ST depression. There is some borderline ST elevation in leads V2 and V3. Similar to case 1, there is ST depression in leads V4-V6. This should be recognized as an EKG diagnostic for LAD occlusion.

A prehospital EKG had been done and is shown below (but has very poor quality)

This shows much ST elevation in anterior leads and illustrates an underrecognized phenomenon: hyperacute T waves are not only present early after occlusion, as the STEMI is developing, but also after the ST segment elevates AND they are present early after reperfusion as the ST segments are falling. They may be the only remaining clue to a reperfused LAD occlusion.

Case 3 (Hyperacute T waves misdiagnosed as Hyperkalemia).

49 yo man with 1 week of stuttering chest burning and tightness for 1-2 hours. Today the discomfort is associated with multiple episodes of vomiting and it is unremittant. The following EKG was obtained and hyperkalemia was diagnosed. The patient was treated with Calcium, Insulin, D50, and bicarbonate, with no change in the ECG. A bedside ultrasound revealed a possible anterior wall motion abnormality. The K returned at 2.9 mEq/L. There was an LAD occlusion that was opened and stented.

These T waves are NOT typical for hyperK. They are "fat" and wide, with a blunt peak and poor R-wave progression (especially V3). The T-waves of hyperkalemia are peaked and tented. See below:


  1. Many thanks for the easy availability of your EKG images. I'm taking my Recertification exam in EM and wanted to get a good feel for the difference between the peaked T in hyperkalemia and the image of hyperacute Ts in early AMI. Your examples are now in my lexicon.

  2. If I'm in an area where PCI is not available, should I initiate thrombolysis in a patient with a typical ACS type chest pain for 3 hours with hyperacute T? Or should I start thrombolysis when it converts to STEMI?

  3. Hyperacute T-waves are considered an indication for thrombolysis. Of course you should be sure that is what is going on. If you are not, wait a bit and get another EKG. The earlier lytics are given, the better they work (fresh clot is busted better than less fresh clot). OK?

    Steve Smith

    1. Do you have a reference for hyper acute t's being an indication for lyrics? Thx in advance.

    2. The 1996 or 2004 (can't remember which) ACC MI guidelines mention it as a consideration. There are no clinical trials of it. There is evidence that hyperacute T-waves are a sign of 1. much myocardium at risk and 2. myocardium that is viable and so can be saved.

  4. Case 3:
    Sir, in V2 and V4 T wave - fat and wide but in V3 it looks like HyperK Twave - tall and tented compare to T wave in V2 and V4

    1. To me it does not look tented, "as if held up by a string". But if you think it is, just measure a potassium!
      Steve Smith

  5. Case 1 and Case 2, ST depression in lead II, what does it signify? Is it reciprocal depression to LAD occlusion?

    1. reciprocal to high lateral STEMI due to LAD occlusion proximal to the first diagonal which supplies the high lateral wall.

  6. I'm working in a centre where PCI is not readily available.
    Can I give lytics to moment I see deWinter T waves in a patient with concerning chest pain?

  7. Yes, it even says so in 2004 STEMI guidelines, the last time it was mentioned:
    Because the benefit of fibrinolytic therapy is directly related
    to the time from symptom onset, treatment benefit is maximized
    by the earliest possible application of therapy. The
    constellation of clinical features that must be present
    (although not necessarily at the same time) to serve as an
    indication for fibrinolysis includes symptoms of myocardial
    ischemia and ST elevation greater than 0.1 mV, in 2 contiguous
    leads, or new or presumably new LBBB on the presenting
    ECG (156,315). In the very early phase of STEMI, giant
    hyperacute T waves may precede ST elevation (316)


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