ECG Blog #514 — Acute Pericarditis?

The ECG in Figure-1 was obtained from a previously healthy middle-aged man — who presented to the ED (Emergency Department) for new CP (Chest Pain).

• The cardiologist on call noted ST elevation in multiple leads — and diagnosed the patient as having acute pericarditis, primarily on the basis of this ECG.

QUESTIONS:

• Do YOU agree with the diagnosis of acute pericarditis?
• If so — Why?  
• If not — Why not?
• 
  
• KEY Point: How to increase the certainty of your diagnosis?

Figure-1: The initial ECG in today’s case.

============================= 

ANSWERS to the above Questions:

The ECG in Figure-1 shows sinus rhythm — with normal intervals (PR-QRS-QTc) and axis — and no chamber enlargement. 

Regarding Q-R-S-T Changes.

• Q Waves — Small and narrow Q waves are seen in multiple leads (ie, in leads II,III,aVF; and in leads V3-thru-V6). Although this is a lot of leads to have Q waves in — the finding that each of these Q waves is small and narrow renders them non-diagnostic.
• R Wave Progression — There is early transition, with the R wave becoming predominant already by lead V2. That said, the clinical significance of this early transition in the context of this tracing is uncertain and non-diagnostic.
• ST-T Wave Changes — There is diffuse ST elevation! In addition to seeing ST elevation in each of the 7 above-noted leads that manifest Q waves — there is also ST elevation in leads I and V2 (ie, which makes for 9/12 leads that show ST elevation).

=============================

The above said — the points made below and the ECG finding that I highlight with YELLOW arrows in Figure-2 explain why I suspected this patient did not have acute pericarditis.

• QUESTION: What do YOU think?

Figure-2: What do the YELLOW arrows highlight?

PEARL #1: The KEY lesson to learn from today’s case — is not to rush to a diagnosis of acute pericarditis in a middle-aged man who presents with new CP. Reasons why I immediately suspected that the diagnosis in today’s case was unlikely to be acute pericarditis include the following:

• Reason #1 = Statistics! — Acute pericarditis is not common. In my experience — acute pericarditis is rare in the clinical setting presented in today’s case (ie, in a previously healthy middle-aged adult — who presents to an ED with new-onset CP). Instead, ACS (an Acute Coronary Syndrome) is a much more common cause of new CP when a middle-aged or older adult presents to the ED with this complaint. As a result, to help me resist the temptation to reflexively diagnose acute pericarditis whenever ST elevation is seen in multiple leads — I embrace (and frequently repeat to myself) the mantra put forth by Dr. Stephen Smith — “You diagnose acute pericarditis at your peril”.

Additional Reasons:

• Today’s case was sent to me with no mention of pertinent positives and pertinent negatives regarding the nature of this patient’s CP. While exceptions exist — the CP of acute pericarditis is typically pleuritic (increasing with inspiration) —and typically positional (exacerbated by lying supine — and reduced by sitting up and leaning forward). The physiologic basis for this positional effect is that lying supine places stretch on the inflamed pericardium — whereas sitting up and leaning forward reduces that stretch.
• There was also no mention of potential predisposing factors that might suggest a diagnosis of acute pericarditis (ie, no known ongoing medical illnesses that may be associated with pericarditis — and no mention of recent viral infection). Although there are many potential causes of pericarditis — the most common clinical setting for acute pericarditis in a previously healthy individual, is in a young adult who presents with an acute viral illness (See the ADDENDUM below).
• Finally — today’s case was sent to me with no mention of having listened for a pericardial friction rub (which IF heard, would confirm the diagnosis of acute pericarditis — albeit not ruling out the diagnosis if not heard).

PEARL #2: When the diagnosis of acute pericarditis is entertained — and the above noted historical and physical exam considerations are not addressed (and not noted in the chart as pertinent positive or pertinent negative findings) — this almost always means that the treating clinician(s) did not completely assess the patient.

• Simply stated — IF the clinician note does not specifically state, "No pericardial friction rub" — this tells me with 99% accuracy that the clinician either did not auscultate the chest specifically listening for a rub and/or simply doesn't appreciate that the BEST (and fastest) way to confirm acute pericarditis is to detect a friction rub. 
• NOTE: See the ADDENDUM below — for more on the clinical and ECG diagnosis of acute pericarditis.

=============================

PEARL #3: The strongest evidence against the diagnosis of acute pericarditis in today's case — is the presence of T-QRS-D (Terminal-QRS-Distortion). In today's initial ECG, this ECG finding is seen in not one — but in multiple leads! ( = the YELLOW arrows in Figure-2).

• I introduced the concept of T-QRS-D in ECG Blog #318. I fully acknowledge that prior to my active participation as an Associate Editor in Dr. Smith's ECG Blog — I had not been aware of this ECG finding. In the years since then, I've seen numerous examples of patient cases that validate the clinical utility of this unique ECG sign promoted by Dr. Stephen Smith. 
• When present — T-QRS-D may provide an invaluable way to distinguish between a repolarization variant vs acute pericarditis vs acute OMI (ie, When true T-QRS-D is present in a patient with new symptoms — it is virtually diagnostic of acute OMI = Occlusion-based Myocardial Infarction). 

I illustrate the ECG finding of T-QRS-D below in Figure-3, — in which I combine figures taken from my ECG Blog #318. To review:

• T-QRS-D — is defined as the absence of both a J-wave and an S-wave in leads V2, V3 and/or lead V4. 
• Although simple to define — this finding may be subtle! I fully acknowledge that it has taken me a while to become comfortable and confident in its recognition.

A picture is worth 1,000 words — as shown in Figure 3:

• TOP in Panel A — Despite marked ST elevation in this lead V3 — this is not T-QRS-D, because there is well-defined J-point notching (BLUE arrow). This patient had a repolarization variant as the reason for ST elevation.
• BOTTOM in Panel A — This is T-QRS-D, because in this V3 lead there is no J-point notching — and, there is no S wave (RED arrow showing that the last QRS deflection never descends below the baseline). 

In Panel B of Figure-3 — I've enlarged the QRST complexes in leads V2 and V3 from the chest leads in this example.

• In Lead V2: The ST elevation is not consistent with T-QRS-D — because there is prominent J-point notching (BLUE arrow).
• In Lead V3: There is T-QRS-D — because there is no J-point notching — and, there is no S wave (RED arrow showing that the last QRS deflection never descends below the baseline).

Figure-3: What is (and is not) T-QRS-D.

=============================

Take Another LOOK at the YELLOW arrows in Figure-2:

Figure-2: Take another look at the YELLOW arrows.

• T-QRS-D — is definitely present in leads V3 and V4 in Figure-2, as there is no J-point notching and there is no S wave (because the last QRS deflection clearly does not descend below the baseline).
• I believe T-QRS-D is also present in lead V2 — although I acknowledge that one might question whether the last QRS deflection reaches the baseline.
• Given definite T-QRS-D in leads V3 and V4 (and probably also in lead V2) — I'd include lead V5 by association. NOTE: Data is lacking to support the validity of T-QRS-D as indication of acute OMI if this finding is only seen in lead V5.
• 
  
• PEARL #4: I added a BLUE arrow in Figure-2 to highlight the ST-T wave in lead aVL. Although very subtle — in the context of seeing T-QRS-D in multiple leads (and considering the tiny size of the QRS in lead aVL) — I believe there is the suggestion of reciprocal ST depression in this lead.
• To emphasize that by itself — I would not think much of the ST-T wave in lead aVL. But in the context of this patient with new CP and T-QRS-D in multiple leads — I interpreted the appearance of lead aVL as showing supportive reciprocal ST depression.

=============================

Take-Home Message: Overall in my experience — T-QRS-D is not a common finding among patients with acute coronary occlusion. That said — the potential value of this finding when it is present, is indisputable (as seen in today's case — in which this ECG finding provides strong support in favor of acute OMI).

=============================

PEARL #5 (Beyond-the-Core): I love PMcardio as a most wonderful application that almost always reliably improves visualization of problematic tracings in a matter of seconds. That said, as helpful as this application is — it is not perfect.

• For example, in today's case — I found that although PMcardio digitalization improved overall resolution of ECG #1 — it rendered the presence of T-QRS-D less evident in several leads by slightly alterating J-point and S wave appearance.
• Bottom Line: As much as I regularly use PMcardio to improve visualization of many imperfect resolution tracings — for fine details in complex arrhythmias and for intricate patterns (such as recognition of T-QRS-D) — it is important that YOU verify the accuracy of the digitalization before blindly accepting the PMcardio version.

=============================

Today's CASE Continues:

Based on the initial strong suspicion of acute pericarditis — a plan was made to treat the patient with colchicine and NSAIDS as antiinflammatory measures.

• However, with the patient still in the ED — VFib (Ventricular Fibrillation) was suddently observed on the monitor. Two defibrillation countershocks were needed to restore sinus rhythm!
• A repeat ECG was obtained after ROSC (Restoration Of Spontaneous Circulation).

QUESTION:

To facilitate comparison between the 2 ECGs in today’s case — I’ve put both of these tracings together in Figure-4.

• What changes have occurred in the post-resuscitation ECG?

Figure-4: Comparison between the 2 ECG in today’s case.

ANSWER:

It should now be obvious that instead of acute pericarditis — today’s patient was in process of evolving an extensive acute STEMI at the time the initial ECG was recorded.

• The repeat ECG shows a marked increase in the amount of ST elevation, and in the hyperacuity of T waves that are seen in virtually all leads.
• Reciprocal ST depression is now obvious in lead III.
• The overall ECG picture in ECG #2 suggests acute LAD occlusion. When the site of occlusion is the proximal LAD — there will often be ST elevation in lead aVL with reciprocal ST depression in one or more of the inferior leads (as is seen in ECG #2).
• I suspect the reason lead aVL showed only very subtle ST depression in ECG #1 (as pointed out in PEARL #4) — is that reciprocal ST depression that was present in lead aVL at that time was attenuated by the onset of opposing ST elevation in this lead that has now become obvious in ECG #2.
• Finally — the occurrence of such diffuse (in 9/12 leads) ST elevation, in association with the surprising findings of such marked ST elevation in lead I — reciprocal ST depression in only one of the inferior leads — and the absence of any ST elevation at all in lead V1 given such marked ST elevation in neighboring lead V2 — suggests the likely presence of underlying multi-vessel coronary disease.

=============================

LEARNING Points:  

• Acute pericarditis is not common. It is much less common than acute coronary disease. As a result, in a patient with new CP — We need to resist the urge to jump to a diagnosis of acute pericarditis until we have ruled out an acute OMI.
• Acute pericarditis is especially unlikely in the absence of predisposing factors (ie, recent or acute viral illness; collagen vascular disease; renal failure, etc.).
• If you consider the diagnosis of acute pericarditis — then you need to carefully listen for a pericardial friction rub.
• 
  
• PEARL #6: I do not know how much time passed between the recording of ECG #1 and ECG #2 in today's case. What we do know — is that given the history of new-onset CP in today's case and the presence of diffuse ST-T wave abnormalities already present in ECG #1 — that a repeat ECG should have been done within no more than 15-20 minutes after ECG #1 was recorded!
• 
  
• PEARL #7: Appreciate the diagnostic utility of T-QRS-D. On occasion (as in today's case) — the KEY ECG finding for confirming the early diagnosis of acute OMI depended on recognition of T-QRS-D.

==================================

Acknowledgment: My appreciation to Ahmed Adel (from Baghdad, Iraq) for submission of today's case.

==================================

=====================================

ADDENDUM (1/17/2026):

• The material that follows below on the ECG diagnosis of acute Pericarditis — is from ECG Blog #365.

—  —

ECG Media PEARL #25 (9:50 minutes Audio) — Pearls & Pitfalls regarding the ECG diagnosis of Acute Pericarditis.

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-4-thru-8.
• 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 Check out ECG Blog #365).

Figure-5: How to make the diagnosis of acute Pericarditis (ie, use of the History and Physical Exam).

Figure-6: ECG findings (4 Stages of acute pericarditis — with attention on diagnostic Stage I). How helpful is PR depression?

 

Figure-7: PR depression (Continued). Spodick’s sign. Acute MI vs Pericarditis vs Repolarization variants?

 

Figure-8: Acute MI vs Pericarditis. ECG findings with acute Myocarditis. Pericarditis vs Early Repolarization?

 

Figure-9: Pericarditis vs Early Repolarization? (Continued).