A 51 yo healthy male had been lifting 5 lb. weights, then went to shower when, at 0800, he developed severe crushing 10/10 left sided chest pain radiating to his left arm that lasted 3 minutes and then mostly, but not completely, subsided. He had SOB and diaphoresis. He went to his clinic and they sent him to the ED. Exam and vital signs were normal. Here is his baseline ECG from 2 years prior:
He had this ECG recorded at 0819:
This was not appreciated, and the patient was set up for a CT coronary angiogram.
The CT results returned hours later showing severe stenosis of both the RCA and LAD. After this, a repeat troponin I returned at 0.51 ng/ml.
Here is a right-sided ECG at 1728. V1(R) = normal V2. V2(R) = normal V1
Subsequently, the patient was treated maximally for NonSTEMI, but developed several episodes of bradycardia, hypotension, and chest pain that was not controlled medically. No ECG ever showed ST elevation or hyperacute T-waves.
Here is the succession of ECGs, side by side, with recording times. aVL is on top, lead III on the bottom:
The patient was taken to the cath lab and had a 99% mid-RCA with enough flow to prevent large infarct. [The STE and large T-wave in V1(R) is not explained by this.] It was opened and stented. The LAD would be fixed later.
Peak cTnI was 15 ng/ml. There was an inferior wall motion abnormality. The patient did well.
Learning points:
1. Serial ECGs are very important
2. New biphasic T-waves are quite specific for ischemia. These are Wellens' waves of the inferior wall.
3. Hemodynamic instability in due to ACS is an indication for immediate angiography and PCI if indicated.
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| Normal. Small normal Q-wave in lead III. |
He had this ECG recorded at 0819:
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| The QRS and T-wave in III are now upright and the T-wave in aVL is flattened |
His initial troponin was normal. He continued to have some chest discomfort, and underwent this ECG at 1024.
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| There is now a prominent Q-wave in lead III with a biphasic T-wave |
This was not appreciated, and the patient was set up for a CT coronary angiogram.
The CT results returned hours later showing severe stenosis of both the RCA and LAD. After this, a repeat troponin I returned at 0.51 ng/ml.
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| The T-wave in lead III is fully inverted now. |
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| There are further dynamic changes in leads III and aVL. The T-wave in V1(R) [V2] is very large, with ST elevation, suggesting RV MI. |
Subsequently, the patient was treated maximally for NonSTEMI, but developed several episodes of bradycardia, hypotension, and chest pain that was not controlled medically. No ECG ever showed ST elevation or hyperacute T-waves.
Here is the succession of ECGs, side by side, with recording times. aVL is on top, lead III on the bottom:
 |
| Ever changing T-waves |
The patient was taken to the cath lab and had a 99% mid-RCA with enough flow to prevent large infarct. [The STE and large T-wave in V1(R) is not explained by this.] It was opened and stented. The LAD would be fixed later.
Peak cTnI was 15 ng/ml. There was an inferior wall motion abnormality. The patient did well.
Learning points:
1. Serial ECGs are very important
2. New biphasic T-waves are quite specific for ischemia. These are Wellens' waves of the inferior wall.
3. Hemodynamic instability in due to ACS is an indication for immediate angiography and PCI if indicated.
Great post Dr. Smith.
ReplyDeleteShould we distinguish between biphasic T waves starting with a positive or negative deflection?
Thank you for your blog,
Miguel Oliveira
Yes. down-up T-waves are usually reciprocal to reperfusion T-waves (up-down) of the opposite (reciprocal) wall. Up-down T-waves are usually reperfusion T-waves of the wall underlying the lead in question.
DeleteSteve Smith