This was sent by a reader who wishes to remain anonymous. Details are at a bare minimum, but it remains instructive.
An elderly patient had a good reason for demand ischemia and there was no suspicion of ACS. This ECG was recorded:
Clinical Course
The pathology leading to the ischemia was treated and resolved. Later, what may have been simply a routine ECG was recorded. If the patient had symptoms at the time of this 2nd ECG, they were not documented. It also is unclear if anyone involved with the patient saw the ECG at the time it was recorded -- no clinician commented on it in the chart.
Here it is:
There is subtle ST elevation in inferior and lateral leads, and subtle reciprocal ST depression in lead aVL and also subtle ST depression in lead V2. This is highly suspicious for acute STEMI, and even meets STEMI criteria in leads V4-V6. It is very unlikely to be pericarditis.
Outcome
Not long after the ECG was recorded, the patient arrested. She was unable to be resuscitated. The autopsy showed an acute RCA thrombosis with 90% occlusion.
Learning Points:
1. You diagnose pericarditis at your (or your patient's) peril
2. Pericarditis does not have reciprocal ST depression, not in either lead aVL or in V2. This ECG is very specific for STEMI.
3. Even when patients are asymptomatic, or apparently so, they can have life threatening MI. If the ECG has specific signs of MI, as this one does, then do not be fooled by the absence of symptoms.
4. It is very easy to overlook ECG findings if you are interpreting a routine ECG, without knowledge of the patient's condition (this includes over-reading of ECGs from a list, as was done in this case).
An elderly patient had a good reason for demand ischemia and there was no suspicion of ACS. This ECG was recorded:
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There is sinus tachycardia. Complexes 3, 6, 12, & 15 appear to have some pre-excitation, with secondary repolarization changes.
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The pathology leading to the ischemia was treated and resolved. Later, what may have been simply a routine ECG was recorded. If the patient had symptoms at the time of this 2nd ECG, they were not documented. It also is unclear if anyone involved with the patient saw the ECG at the time it was recorded -- no clinician commented on it in the chart.
Here it is:
 |
| The cardiologist who read the ECG on the system (who probably did not know the patient or the reason for the recording) read this as "Diffuse Nonspecific ST Elevation, consider Pericarditis" What do you think? |
There is subtle ST elevation in inferior and lateral leads, and subtle reciprocal ST depression in lead aVL and also subtle ST depression in lead V2. This is highly suspicious for acute STEMI, and even meets STEMI criteria in leads V4-V6. It is very unlikely to be pericarditis.
Outcome
Not long after the ECG was recorded, the patient arrested. She was unable to be resuscitated. The autopsy showed an acute RCA thrombosis with 90% occlusion.
Learning Points:
1. You diagnose pericarditis at your (or your patient's) peril
2. Pericarditis does not have reciprocal ST depression, not in either lead aVL or in V2. This ECG is very specific for STEMI.
3. Even when patients are asymptomatic, or apparently so, they can have life threatening MI. If the ECG has specific signs of MI, as this one does, then do not be fooled by the absence of symptoms.
4. It is very easy to overlook ECG findings if you are interpreting a routine ECG, without knowledge of the patient's condition (this includes over-reading of ECGs from a list, as was done in this case).
Highly illustrative case. You will go down in ECG lore with your prophetic quote, “You diagnose pericarditis at your (or your patient’s) peril” — as you have previously on your Blog shown other such cases when a diagnosis of "pericarditis" comes back to haunt ... This should be ESPECIALLY true when a diagnosis of acute pericarditis is contemplated in an older patient like this one — as acute viral pericarditis is not at all common in that setting. I agree with your interpretation of this 2nd tracing. Lead aVL is certainly a key (it shouldn’t be depressed with simple pericarditis) — and V2 (as you indicate) should show ST elevation. I’d interpret the ST-T changes in V1 almost as a Brugada pattern (doubtless phenocopy given impending cardiac arrest).
ReplyDeleteAs to the ongoing change in QRST morphology almost every-third-beat in the TOP tracing — rather than intermittent preexcitation (I don’t see delta waves), I’d suspect either: i) electrical alternans (which can occur with ischemia and/or LV dysfunction); or more likely ii) Ventricular trigeminy. The difficulty lies in determining IF the PR interval changes. It looks like the PR interval may be a bit shorter for the 3rd beat — though amidst all the baseline artifact it is hard to tell if there is shortening of the PR for the other beats. My hunch is that this is ventricular trigeminy with end-diastolic PVCs that are common with reperfusion — in this patient with impending cardiac arrest … These are often hard to recognize when the PVCs are “end-cycle”, as resultant fusion with the near-simultaneously occurring sinus beat leads to close resemblance to normal beats.
THANKS for posting this insightful case Steve!
Thanks, Ken! You don't think that upstroke is a delta wave?
DeleteI don't think there are delta waves here Steve — and, I have been fooled more than once in the past by end-diastolic PVCs that fuse with the underlying sinus rhythm ... and, without any preceding history of WPW in this older patient, I would think ventricular ectopy a far more likely possibility in this ischemic setting ... That said, we clearly would need more history and tracings in order to know for certain. THANKS again for posting this excellent case!
ReplyDeleteI cant comment much on AvR in this ECG as QRS is keep changing its morphology due to pre-excitation/ventricular rhythm. correct me If I am wrong but I guess there is ST-Elevation in AvR too. this could suggest LM stenosis leading to this later event. Althu Autopsy is suggesting otherwise.
ReplyDeleteThe FIRST ECG has STE in aVR. STE in aVR is simply reciprocal to ST depression directed towards the cardiac apex. It most commonly is seen in NON-ACS ischemia. see this post: http://hqmeded-ecg.blogspot.com/2014/08/the-difference-between-left-main.html
DeleteST elevation is ST elevation. Don't ignore it. The second ECG is IMO one hundred percent acutely ischaemic, not at all charataristic of Pericarditis.
ReplyDeleteDr. Smith - Yet another instructive post. Can you comment please on the inferior T-waves in the second EKG. Are they borderline hyperacute?
ReplyDeleteThank you so much for your teaching efforts, it is truly appreciated.
No doubt about it!!
Deletethank you!
Steve Smith