Wednesday, November 26, 2014

An elderly man with severe chest pressure......

This was sent to me by a medical student:

The patient is an elderly man with no significant past medical history who developed what he describes as chest tightness throughout his anterior precordium, 9/10 in severity, associated with nausea, vomiting, diaphoresis and shortness of breath, lasting for greater than 2 hours, that started while he was lifting firewood. His symptoms did not go away with rest. He presented to his primary care physician's office. An EKG was recorded at 135 minutes after pain onset:
There is no old ECG for comparison.  What do you think?



He was treated with sublingual nitroglycerin and aspirin, which improved his chest discomfort. He was transported by ambulance to the hospital. On initial evaluation in the emergency department he still had pain and had this ECG recorded at 150 minutes (2.5 hours) after pain onset: 
What do you think?  See below.















The med student asked what I thought, and I wrote: "hyperacute T-waves in V4-V6."  Here is the normal relationship between the T-waves and the QRS in V4-V6:
Knowing this is the normal proportion, what do you NOW think about the above 2 ECGs?

It is clear that the T-waves in V4-V6 on the first two ECG are hyperacute.  They are far too large for the QRS.  In addition, if you look closely, you will see that there is more ST elevation on the second ECG.  In fact, on the 1st ECG, V5 had zero ST elevation but has almost 2 mm on the 2nd ECG.

These findings, along with the pretest probability (a 77 year old with persistent substernal chest pressure and diaphoresis!!) mandate at least a stat formal echo, but preferably emergent coronary angiography


Initial cardiac markers were negative. The patient became chest pain-free.  


He was admitted for a "rule out."


A cardiologist evaluated his ECGs:


"In the emergency room an EKG was obtained which showed Q-waves throughout the precordial leads and some reciprocal mild ST elevations but with a distinct J-point and less than 1 mm STE.  I was asked to see the patient and review the ECGs and I felt this represented old anterior MI which had been completed at some point in the remote past."  


I do not fully understand this explanation.


He underwent more ECGs: 200 minutes (2 hours 40 min) after pain onset: 

Complexes 8 and 12 are PVCs. R-waves in leads V4-V6 are much diminished and T-waves are not nearly as tall as they were.
At 270 minutes (4.5 hours) after pain onset, the patient reported a slight increase in pain, and another ECG was recorded:
Now there is ST elevation in V4-V6, the T-waves are still large, and there is poor R-wave progression

The cardiologist wrote this note:


“Pt reported a slight increase in pain. Repeat EKG showed no clear ischemic changes. Old Q waves.”  
At 10.75 hours after the pain onset, the pain was increasing.  Troponin I returned at 7.42 ng/mL.  This ECG was recorded:
Well developed infarction with QS-waves, diminishing T-waves and some terminal T-wave inversion


Another ECG was recorded at 13 hours after pain onset: 
Deepening T-wave Inversion


At 15 hours after the first ECG, the patient was taken for angiogram and had a 100% distal LAD occlusion.  It was opened and stented.

Here is the post cath ECG:
There is deepening T-wave inversion.



Peak troponin I = 29 ng/mL.  Formal echo shortly after the stent placement showed a dyskinetic anterior wall and an EF of 35-40%.


Learning Points

1. T-waves should be proportional to the QRS.  If they are too large, you must suspect hyperacute T-waves and aggressively evaluate the patient with at least a high quality emergent echocardiogram

2. When the ECG is diagnostic, as here, do not wait for troponins to be positive before acting.  Most coronary occlusion has initially negative biomarkers.  Once the troponins are positive, much damage is done.

9 comments:

  1. Have posted my comment in facebook, but nevertheless
    Does the culprit artery affect inferior wall as well?
    In the first ECG, isnt T wave in lead II hyperacute to QRS as well?
    In avF, there is a QS pattern there too. In III, there is (what i think) is inverted T wave

    During the third ECG, we can see the T in III actually coming up, then slowly flattens in the next ECG

    ReplyDelete
    Replies
    1. Ryan,
      Yes, I and II both also have probable hyperacute T's, and I actually wrote that to the student as well. QS in III can be normal due to axis only, and a QS should have a negative T-wave.
      I don't know if the culprit affected inferior wall, but I would expect more hyperacute T in III if it did.
      Thanks!
      Steve

      Delete
  2. is there an inferior involevement ? T wave seems to be out of proportion in lead II and there's also ST elevation in that lead later ?

    Thank you very much .

    ReplyDelete
    Replies
    1. ben, see above comment and response!
      Steve

      Delete
  3. This is a classic case where bedside ultrasound would have likely made a huge difference. The ability to teach ultrasound to clinicians is readily available and has been included in the curriculum of many medical schools and residency programs. Just a quick look at this patient's anterior wall function on ultrasound early in his course would have given all the information anyone needed to go the cath lab immediately. Why are we relying on stethoscopes and ECG's alone to evaluate cardiac function at the bedside? It's 2014.

    ReplyDelete
    Replies
    1. Cookie,
      Absolutely. That is what I do. Here are a bunch of posts in which the ECG findings are greatly enhanced by bedside echo: http://hqmeded-ecg.blogspot.com/search/label/echocardiogram.
      Thanks!
      Steve

      Delete
  4. Your 2 learning points about this case reflect the essential basics that should be remembered. They are totally obvious on this case. I cringed when reading the consultant cardiologist's notes. There are important lessons in this case to be learned for all (consulting cardiologist included). THANKS for posting.

    ReplyDelete
  5. Dear Dr. Smith, I notice that there is definite and progressive loss of R waves at the lateral leads starting with the 3rd ECG. A very important clue as to the nature of the chest pain, that must be.

    I am also a bit surprised to see a lateral MI as a consequence of an LAD lesion.

    Lastly, do we have;
    - an ECHO ?
    - a tracing taken right after the patient became pain-free (so that it might be possible to see the hyperacute lateral waves temporarily reverting to normal, which would be another proof of a developing STEMI) ?

    There may not be any other ECG site on the internet as informative as yours. Simply excellent. Thank you very much.

    Dr. Mehmet K. Çelenk

    ReplyDelete
    Replies
    1. Thank you Dr. Celenk,
      I do not have an echo available, but there was LV gram:
      "Right anterior oblique LV gram demonstrates normal chamber size. There is dyskinetic movement of the left ventricular apex. Remaining walls contract normally. The overall LVEF appears mild to moderately reduced. The EF is about 35-40%."
      V5 and V6 are often slightly misplaced at the apex, or the apex is slightly more lateral than normal. In either case, they will represent apical ischemia, as here.
      Of course a proximal LAD occlusion will affect the lateral wall via its disruption of first diagonal flow.
      Unfortunately, I have posted all the ECGs that were recorded prior to cath.
      Steve Smith

      Delete

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