First, I want you to see the ECG without a lot of clinical information: this 45 year old male presented with left chest pain:
More clinical information:
One week prior, he was stabbed in the left chest and a chest tube was placed. His pulse was 120 and blood pressure 90/50.
ECG analysis:
There is sinus tachycardia. There is ST elevation in inferior, lateral, and anterior leads. The ST elevation in II is greater than III. There is no reciprocal ST depression in aVL. The ST elevation in anterior leads is marked, and scary. There is perhaps excessive PR depression (see esp. leads II, V5). This ECG is classic for pericarditis, but could conceivably be due to antero-infero-lateral STEMI due to proximal (before D1 to the lateral wall) occlusion of a type III (wraparound, to inferior wall) LAD.
Findings favoring pericarditis over diffuse MI:
1) no ST depression in aVL. We studied 160 inferior STEMI; only 1 had absence of any ST depression in aVL. We also studied 39 consecutive cases of pericarditis who presented to the ED with chest pain and ST elevation meeting "reperfusion criteria." None had any ST depression anywhere (except aVR, in which all had it).
2) The computerized QTc is 371 ms. This makes anterior MI very unlikely. In my study of 355 consecutive LAD occlusions, only 2 had a QTc less than 372 ms.
3) High anterior R-wave amplitude. The mean R-wave amplitude in V2-V4 is at least 18 mm. In my study of 355 consecutive LAD occlusions, zero had a mean R-wave amplitude this high.
4) STE in lead II greater than lead III. This is not very accurate, and is found in inferior MI due to circumflex occlusion; i.e., inferolateral MI may have this.
5) The equation value (incorporating ST elevation, R-wave amplitude, and QTc) is 22.32 (less than 23.4 is unlikely to be LAD occlusion when early repol is the alternate diagnosis, but this has not been tested against pericarditis)
I was shown this ECG with no clinical info the next day, and due to the above considerations, after a glance at the ECG I said, "It's not an MI."
Verifying the diagnosis of pericarditis by ED bedside echo
If this is STEMI, it is a massive antero-infero-lateral STEMI and the patient would probably present in cardiogenic shock. A bedside echo should show very poor LV function, and the patient should probably have pulmonary edema (which he did not). A bedside echo was done: there was no pericardial effusion and, though the LV was not what the clinicians thought should be appropriately hyperdynamic, there was only "possibly decreased LV function."
Further evaluation revealed a fever of 101. Fluids were given and the heart rate decreased, but an ECG 30 minutes later was unchanged. The cath lab was activated. Ultimately, he was not taken to the cath lab and troponins had a very tiny rise consistent with a very small degree of myocarditis in addition to pericarditis. He grew out MSSA from his blood and had an infected hematoma in his chest. The next day, he developed a pericardial friction rub, confirming the diagnosis of myo-pericarditis. No more ECGs were recorded.
Here are more cases in which pericarditis was on the differential diagnosis.
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| What do you think? |
More clinical information:
One week prior, he was stabbed in the left chest and a chest tube was placed. His pulse was 120 and blood pressure 90/50.
ECG analysis:
There is sinus tachycardia. There is ST elevation in inferior, lateral, and anterior leads. The ST elevation in II is greater than III. There is no reciprocal ST depression in aVL. The ST elevation in anterior leads is marked, and scary. There is perhaps excessive PR depression (see esp. leads II, V5). This ECG is classic for pericarditis, but could conceivably be due to antero-infero-lateral STEMI due to proximal (before D1 to the lateral wall) occlusion of a type III (wraparound, to inferior wall) LAD.
Findings favoring pericarditis over diffuse MI:
1) no ST depression in aVL. We studied 160 inferior STEMI; only 1 had absence of any ST depression in aVL. We also studied 39 consecutive cases of pericarditis who presented to the ED with chest pain and ST elevation meeting "reperfusion criteria." None had any ST depression anywhere (except aVR, in which all had it).
2) The computerized QTc is 371 ms. This makes anterior MI very unlikely. In my study of 355 consecutive LAD occlusions, only 2 had a QTc less than 372 ms.
3) High anterior R-wave amplitude. The mean R-wave amplitude in V2-V4 is at least 18 mm. In my study of 355 consecutive LAD occlusions, zero had a mean R-wave amplitude this high.
4) STE in lead II greater than lead III. This is not very accurate, and is found in inferior MI due to circumflex occlusion; i.e., inferolateral MI may have this.
5) The equation value (incorporating ST elevation, R-wave amplitude, and QTc) is 22.32 (less than 23.4 is unlikely to be LAD occlusion when early repol is the alternate diagnosis, but this has not been tested against pericarditis)
I was shown this ECG with no clinical info the next day, and due to the above considerations, after a glance at the ECG I said, "It's not an MI."
Verifying the diagnosis of pericarditis by ED bedside echo
If this is STEMI, it is a massive antero-infero-lateral STEMI and the patient would probably present in cardiogenic shock. A bedside echo should show very poor LV function, and the patient should probably have pulmonary edema (which he did not). A bedside echo was done: there was no pericardial effusion and, though the LV was not what the clinicians thought should be appropriately hyperdynamic, there was only "possibly decreased LV function."
Further evaluation revealed a fever of 101. Fluids were given and the heart rate decreased, but an ECG 30 minutes later was unchanged. The cath lab was activated. Ultimately, he was not taken to the cath lab and troponins had a very tiny rise consistent with a very small degree of myocarditis in addition to pericarditis. He grew out MSSA from his blood and had an infected hematoma in his chest. The next day, he developed a pericardial friction rub, confirming the diagnosis of myo-pericarditis. No more ECGs were recorded.
Here are more cases in which pericarditis was on the differential diagnosis.
Excellent discussion, as usual
ReplyDeletePierre, from France
Thank you, Pierre. By the way, for those of you who read French (and, even if you don't, Google Translate will translate it for you), see Pierre's excellent ECG site:
ReplyDeletehttp://www.e-cardiogram.com/
Dr. Smith,
ReplyDeleteI also noticed slight PR depression and notched J-points. Garcia and Holtz states that if you find notched J-point elevation there's a 99% chance that its from a benign origin
That may be true in inferior leads (what is their reference?), but in our study of anterior STEMI vs. early repol it was not true.
ReplyDeleteAnd I mean what is the study, with data, that it comes from? Or is this from a textbook? I tend to put a lot of weight on notching in inferior leads, and have wanted to study it, but it is not easy. Is there actually a published study of good quality that shows this?
ReplyDeleteOn your 6/18/2011 post (http://hqmeded-ecg.blogspot.com/2011/06/transient-stemi-serial-ecgs-prehospital.html), you state that pericarditis doesn't have hyperacute T waves. These T waves seem hyperacute to me. Is this an exception to the rule or am I mistaken in calling these hyperacute? Thanks
ReplyDeleteI would say these are not hyperacute T-waves because T-waves must be assessed in proportion to the QRS, which here has very high voltage. In the other case you mentioned, the voltage is not nearly as high.
DeleteOK?
Steve Smith
I really enjoyed this case. Thank you so much.
ReplyDelete