Written by Pendell Meyers
Try first to interpret the ECG without any clinical context:
What do you think? |
Sinus rhythm with abnormal STE in V2-V6, and I, II, aVF. Reciprocal STD in aVR and V1. Most leads with STE have remarkably non-hyperacute, flat T waves. Most would say that there is Spodick's sign. The PR depression in II (and its reciprocal PR elevation in aVR) is probably beyond normal baseline values. Overall, this looks like one of the rare ECGs that is actually specific for pericarditis in my opinion. There was no prior ECG for comparison. Of note, there is arguably terminal QRS distortion in V4-V6.
QOH versions 1 and 2 both say Not OMI, with high confidence, without any clinical context, despite the abnormal STE meeting STEMI criteria.
I sent this to our group without information and Dr. Smith responded: "Not OMI. Pericarditis maybe."
Context: a man in his 40s presented to the emergency department with 1 day of sudden onset chest pain. Two weeks ago he had a significant MVC with many severe injuries, including aortic injury s/p endovascular repair.
Echo showed a new large pericardial effusion with large focal hematoma in the posterior pericardium near the descending thoracic aorta/TEVAR edge. CT angiogram showed stable TEVAR without complications. Serial echo monitoring showed increasing pericardial pressures without overt tamponade physiology. ESR and CRP were both highly elevated. Serial high sensitivity troponins were negative. Pericardiocentesis was performed. He was concomitantly treated with colchicine and NSAIDs.
Here was another ECG done later:
The patient did well.
MY Comment, by KEN GRAUER, MD (8/4/2024):
- i) Today's case provides an example of an initial ECG, that in Dr. Meyers' words — "is one of the rare ECGs that is actually specific for pericarditis". The clinical reality is that the overwhelming majority of cases in Dr. Smith's ECG Blog, in which acute pericarditis is strongly considered as the diagnosis based on ECG findings — turn out not to be the result of pericarditis.
- ii) Today's case emphasizes the importance of the history in making the diagnosis of pericarditis.
- iii) Finally — Today's 2 ECGs provide insight into the art of comparing serial tracings.
- NOTE: By way of reference — I've added below an ADDENDUM excerpted from My Comment in the May 16, 2023 post in Dr. Smith's ECG Blog, summarizing "My Take" regarding diagnostic considerations for pericarditis.
Figure-1: For ease of comparison — I've put together the 2 ECGs in today's case. (To improve visualization — I've digitized the original ECG using PMcardio). |
- There is diffuse ST elevation (seen in 9/12 leads) — with the only leads not showing ST elevation being right-sided leads III, aVR and V1.
- There is marked PR segment depression in multiple leads (best seen in leads I,II,aVF) — with PR segment elevation in lead aVR.
- The ST-T wave in Lead II looks more like lead I than lead III (whereas the opposite is true with acute inferior MI).
- Infarction Q waves are absent.
- There is no localization of ST elevation, as is typically seen with acute MI. With the possible exception of lead V2 — the hyperacute appearance of T waves typical of acute MI is lacking. Instead (as per Dr. Meyers) — most T waves are remarkably flat (and the reason for the shape of the ST-T wave in lead V2 may be a result of LV "strain" in an anterior lead of a patient with voltage for LVH).
- T waves are not inverted in leads that manifest ST elevation (whereas the opposite often occurs with acute MI).
- Spodick sign is present.
- The ST/T wave ratio (ie, the ratio of ST elevation compared to T wave amplitude) in lead V6 is well over 0.24 (See My Comment in the June 8, 2022 post for more on this Ratio).
- Clinical symptoms of pericarditis (ie, positional and/or pleuritic chest pain) — as well as ECG findings are not necessarily the same for all of the potential etiologies listed above (ie, some patients may even be asymptomatic — and typical ECG findings of pericarditis are not uniformly present).
- Echo is most often normal in patients with the most common form of acute pericarditis (which is acute viral pericarditis). In contrast — pericardial effusion (which may be large) becomes much more likely with pericarditis from many of the other etiologies listed above (as was the case for today's patient).
- In today's case, as soon as the history became known (ie, that 2 weeks earlier the patient suffered severe injuries following a motor vehicle accident — including aortic injury which was surgically repaired) — it became evident that rather than an acute cardiac event — the markedly abnormal findings in ECG #1 were the result of pericarditis (with the positive ESR and CRP inflammatory markers in today's case serving to distinguish between simple traumatic or post-operative pericardial effusion — vs a component of pericardial inflammation).
- Bottom Line: Attention to details in the history relative to any of the above potential etiologies of pericarditis — is essential for making this diagnosis.
- Part of the reason for the seemingly increased T wave size in ECG #2 — may be a result of pericardiocentesis of the large pericardial effusion.
- A more likely reason is the change in QRS morphology in the precordial leads. In ECG #1 — transition occurs much earlier (between leads V3-to-V4) — with tall, monophasic R waves in leads V4,V5,V6.
- In contrast in ECG #2 — transition is delayed until between leads V5-to-V6, and tall, predominant R waves are never established. Given that pericardiocentesis had just been done — were bandages or other impediment to normal precordial lead electrode placement the reason for the change in ST-T wave appearance?
- Take-Home Point: Comparison of serial tracings is an art. This practice is best done with both ECGs being compared placed next to each other (as in Figure-1). The fact that there is no appreciable change in the frontal plane axis between ECG #1 and ECG #2 tells us that lead-by-lead comparison of ST-T wave appearance in the limb leads will be an accurate indicator. In contrast — the obvious difference in R wave progression between the 2 tracings in Figure-1 has to be taken into account when trying to determine if differences in ST-T wave morphology are (or are not) the result of some dynamic ischemic change.
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ADDENDUM (8/3/2024): In the following 5 Figures — I post written summary from my ECG-2014-ePub on the ECG diagnosis of Acute Pericarditis.
- CLICK HERE — for a PDF of this 9-page file on Pericarditis that appears in Figures-2-thru-6.
- An additional criterion that has sometimes been cited as helpful for making the diagnosis of acute Pericarditis — is the ST/T Wave Ratio in Lead V6 (Please see My Comment at the BOTTOM of the page in the December 13, 2019 post of Dr. Smith's ECG Blog).
Figure-2: How to make the diagnosis of acute Pericarditis (ie, use of the History and Physical Exam). |
Figure-3: ECG findings (4 Stages of acute pericarditis — with attention on diagnostic Stage I). How helpful is PR depression? |
Figure-4: PR depression (Continued). Spodick’s sign. Acute MI vs Pericarditis vs Repolarization variants? |
Figure-5: Acute MI vs Pericarditis. ECG findings with acute Myocarditis. Pericarditis vs Early Repolarization? |
Figure-6: Pericarditis vs Early Repolarization? (Continued). |
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