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.

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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).

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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.

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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.

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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.

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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).

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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.

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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.

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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.

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

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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).

ECG Blog #513 — Trauma and What Else?

The ECG in Figure-1 was obtained from a previously healthy middle-aged woman who was involved in a severe MVA (Motor Vehicle Accident). She was being resuscitated per trauma protocol — and she was hemodynamically stable at the time this tracing was recorded.

QUESTION:

• Given the above clinical setting — How would you interpret the ECG in Figure-1?

Figure-1: The initial ECG in today's case. The patient was in a severe MVA.  (To improve visualization — I've digitized the original ECG using PMcardio).

My Thoughts on Figure-1:

Given the history of involvement in a severe MVA — I immediately considered a cardiac contusion as contributing to the abnormal ECG in Figure-1.

• The rhythm is a regular WCT (Wide-Complex Tachycardia) at a rate of ~130/minute. I suspected that the regular upright deflections preceding each QRS complex in lead II were sinus P waves (broken line RED arrows in this lead in Figure-2).
• Seeing similar upright deflections preceding each QRS complex in neighboring lead I at the same moment in time — is in support of the likelihood that the rhythm is sinus tachycardia.
• That said, given the rapid rate and the presence of small deflections that appear to notch the ST segments midway between the RED arrows in lead II (broken line BLUE arrows in Figure-2) — I could not rule out the possibility of 2:1 atrial activity, as might occur with atrial flutter. I also did not clearly see sinus P waves in either lead V1 or V2, as I would expect with sinus tachycardia.

As noted — the QRS looks wide.

• To Emphasize: QRS morphology is consistent with RBBB (Right Bundle Branch Block) — given the qR pattern in lead V1 — with wide terminal S waves in lateral leads I and V6.
• Therefore, at the least — this regular WCT rhythm is almost certain to be supraventricular. I could not completely rule out the possibility of 2:1 conduction — but strongly suspected the rhythm was indeed sinus tachycardia (ie, The history of a traumatic MVA is certainly consistent with sinus tachycardia — without having to postulate another form of tachyarrhythmia).
• 
  
• PEARL #1: When we suspect a given etiology for the rhythm (as I suspected sinus tachycardia for the rhythm in Figure-2) but we are not 100% certain of that diagnosis — it is best to reserve final judgement until we are able to approach 100% certainty. 
• Practically speaking — our initial management of today’s patient will not be different regardless of whether we are dealing with sinus tachycardia, ATach or AFlutter (ie, In all 3 situations — We would continue protocols for trauma assessment and treatment until such time that we better appreciate the extent of this patient’s injuries). And, if the rhythm is sinus tachycardia — the heart rate will almost certainly decrease with fluid resuscitation and other treatment measures.

Figure-2: I’ve labeled potential signs of atrial activity in leads I and II.

What Else do We See on Today’s Initial ECG?

There are many additional findings to be concerned about on today’s initial ECG — which I’ve highlighted in Figure-3: 

• There is extremely low voltage in 10/12 leads (ie, in all leads except V1,V2 — in which the reason the R wave may be as tall as it is in leads V1,V2 — may simply be a reflection of delayed and independent depolarization of the right ventricle, as physiologically occurs when there is RBBB).
• PEARL #2: As suggested in ECG Blog #272 — among the causes of Low Voltage is low cardiac output, as may occur as a result of a large MI (or in today’s case, as a result of a significant cardiac contusion).
• 
  
• There are also diffuse QRST abnormalities that are seen in virtually every lead in this tracing.

Regarding Q-R-S-T Wave Changes:

• Q Waves — are present in multiple leads ( = the 5 YELLOW arrows in Figure-3). These include leads V1,V2 (ie, loss of the initial positive r wave deflection that should normally be seen in these leads with RBBB) — in neighboring leads V3,V4 (In addition to tiny voltage in these leads — there is absence of any initial positive r wave deflection) — and in lead aVL (which manifests a relatively large Q wave given tiny size of the QRS).
• R Wave Progression — is altered by the tall R waves in V1,V2 from the RBBB — but thereafter is marked by loss of R wave amplitude, with transition never occurring (ie, R wave amplitude remains smaller than the S wave is deep across the precordium, extending to lead V6).

Regarding ST-T Wave Changes: 

• There is marked ST elevation in leads I and aVL (within the RED rectangles in these leads in Figure-3). Equally marked reciprocal ST depression is seen in each of the inferior leads (BLUE arrows in these leads).
• Marked ST elevation is also seen in lead aVR.
• To Emphasize: Considering tiny size of QRS amplitude in the limb leads — the relative amount of ST segment deviation (elevation and depression) is enormous.

ST-T wave changes in the chest leads are more subtle:

• Normally with RBBB — the ST-T wave will be oppositely directed to the positive terminal R wave. Instead, there is subtle-but-significant ST elevation in lead V1 – with more marked ST elevation in lead V2 (within the RED rectangle in these leads).
• The unsteady baseline makes assessment more difficult for ST-T wave changes in leads V3,V4,V5. But especially considering tiny size of the QRS in lead V6 — there is significant ST depression in this lead (BLUE arrows in lead V6). 

Impression of ECG #1: If the history associated with this tracing was that of new chest pain — our impression would be that an extensive STEMI was ongoing, with tachycardia, developing Q waves in many leads, RBBB and marked low voltage — all of which suggest cardiogenic shock.

• Given the history of a severe MVA — these ECG findings could all be explained by MVA-related trauma causing Cardiac Contusion.
• And/or — the trauma and stress of the accident may have also precipitated either an acute MI and/or Stress Cardiomyopathy (which would be consistent with what appears to be QTc prolongation).
• ST elevation in lead aVR, in association with marked inferior lead ST depression and ST depression in lead V6 — may reflect DSI (Diffuse Subendocardial Ischemia). DSI is not an unexpected finding given the rapid heart rate and diffuse myocardial injury pattern seen in today's initial ECG (See ECG Blog #483 — for more on DSI).

Figure-3: In addition to diffuse low voltage — I've highlighted multiple Q-R-S-T abnormalities in the initial ECG.

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What are the ECG Findings of Cardiac Contusion?

Overall — the ECG is less than optimally sensitive for detecting cardiac injury following blunt trauma. This is because the anterior anatomic position of the RV (Right Ventricle), and its immediate proximity to the sternum — makes the RV much more sussceptible to blunt trauma injury than the LV. But because of the much greater electrical mass of the LV — electrical activity (and therefore ECG abnormalities) from the much smaller and thinner RV may sometimes be more difficult to detect.

PEARL #3: Regarding ECG findings with Cardiac Contusion (using the following sources — Sybrandy et al: Heart 89:485-489, 2003 — Alborzi et al: J The Univ Heart Ctr 11:49-54, 2016 — and Valle-Alonso et al: Rev Med Hosp Gen Méx 81:41-46, 2018) — I found the following ECG findings to be most commonly reported.

• None (ie, The ECG may be normal — such that not seeing any ECG abnormalities does not rule out the possibility of cardiac contusion).
• Sinus Tachycardia (common in any trauma patient … ).
• Other Arrhythmias (PACs, PVCs, AFib, Bradycardia and AV conduction disorders — potentially lethal VT/VFib).
• RBBB (as by far the most common conduction defect — owing to the more vulnerable anatomic location of the RV). Fascicular blocks and LBBB are less commonly seen.
• Signs of Myocardial Injury (ie, Q waves, ST elevation and/or depression — with these findings suggesting LV involvement).
• QTc prolongation (with the QTc looking "long" in Figure-3 — albeit much harder to accurately determine the QTc in today's initial ECG given the tachycardia).

Additional Important Points:

• Prediction of cardiac contusion “severity” on the basis of cardiac arrhythmias and other ECG findings — is an imperfect science.
• Despite the predominance for RV (rather than LV) injury — use of a right-sided V4R lead has not been shown to be helpful (compared to use of a standard 12-lead ECG for detecting ECG abnormalities).
• In addition to ECG abnormalities related to the blunt trauma of cardiac contusion itself — Keep in mind the possibility of other forms of cardiac injury in these patients (ie, valvular injury, aortic dissection, septal rupture) — as well as the possibility of a primary cardiac event (ie, acute MI may have been the cause of an accident that led up to the trauma).
• ECG abnormalities may be delayed — so repeating the ECG if the 1st tracing is normal is appropriate when concerned about severe traumatic injury.
• The "good news" re assessing risk when cardiac contusion is suspected in association with acute trauma — IF troponin is normal at 4-6 hours and IF the ECG is normal — then the risk of cardiac complications is extremely low.

Bottom Line regarding Today's CASE:

Given the multiple ECG abnormalities described above in today's initial ECG — significant cardiac involvement is obvious. Whether this is the purely the result of cardiac contusion and/or whether an acute MI is also implicated — would not be known solely from review of the initial ECG.

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PEARL #4: An Often-Ignored ECG Finding ...

We do not usually think of the ECG as a way of estimating a patient's respiratory rate. That said — awareness that on occasion we can estimate how fast the patient is breathing may at times be extremely helpful.

• This is especially true when charged with interpreting the ECG of a patient we have not seen. For example — the ECG suggestion of tachypnea may clue us in to a patient with respiratory difficulty who needs to be immediately seen.

Consider Figure-4 — in which I've magnified the view of leads V1,V2,V3 from the initial ECG in today's case.

• Note the rhythmic rise-and-fall in the baseline seen every 3 QRS complex.
• When you see a consistent rise and fall of the baseline occurring at a fixed interval over a majority of the 12-lead recording — this most probably reflects the patient's respiratory rate (to be distinguished from the much more common random baseline variation — from which the patient's respiratory rate can not be accurately assessed).
• In Figure-4 — 2 breaths are seen to occur over a period of 2.8 seconds (ie, over a period of 14 large boxes). This means that 1 breath occurs over a period of 1.4 seconds — and 60 sec./min. ÷ 1.4 seconds = tachypnea at a respiratory rate of ~43/minute (which is not surprising given that the initial ECG suggests this patient is in shock).

Figure-4: Use of the ECG to estimate respiratory rate.

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Today's CASE Continues:

The patient was resuscitated by trauma protocol:

• Musculoskeletal injuries were treated.
• The patient received blood products.
• She was intubated to secure the airway — followed by additional fluid resuscitation and sedation.
• Serum electrolytes were normal.
• Bedside Echo suggested anterolateral akinesis (consistent with the very low voltage and anatomic distribution of Q waves and ST elevation).

Minutes later — the patient developed the rhythm shown in Figure-5.

• QUESTION: What has happened?

Figure-5: The patient suddenly developed the rhythm shown in the chest leads.

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MY Thoughts on the ECG in Figure-5:

A total of 26 beats are seen in ECG #2 — with the first 9 beats appearing in the limb leads.

• The limb leads show little change since ECG #1 — with sinus tachycardia again suggested as the underlying rhythm (at the same very rapid rate of ~130/minute). We once again see very low voltage — with a similar amount of ST elevation in leads I,aVL and reciprocal ST depression in the inferior leads.
• Beat #10 is partially hidden by the lead change border.
• Beat #11 is the first complete beat seen in the chest leads. It shows the same RBBB morphology (with initial Q wave and similar ST elevation in leads V1,V2). Looking down at simultaneously-occurring beat #11 in the long lead II rhythm strip (at the bottom of the tracing) — we can see that beat #11 is sinus-conducted (the RED arrow preceding beat #11 in the long lead II rhythm strip).
• Note that P waves are lost in the long lead II after beat #11.
• Turning our attention to lead V1 — a 13-beat run of a very different-looking WCT rhythm begins with beat #12. The rate of this almost regular WCT rhythm is over 200/minute. The very wide and amorphous QRS morphology in leads V1 and V2, along with marked change in QRS morphology during this 13-beat run in leads V3,V4,V5 is virtually diagnostic of VT (Ventricular Tachycardia).
• QRS morphology almost normalizes for the last 2 beats in this tracing ( = beats #25,26) — suggesting that the run of VT may be terminating (although we are not privy to what happens after beat #26).

Figure-6: I've numbered the beats and have labeled P waves.

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CASE Follow-Up:

The patient had several episodes of NSVT (Non-Sustained VT ).

• Over the ensuing days — the patient's condition stabilized. VT episodes ceased. She remained on ventilator support. Echo documented an EF ~25-30%.
• Unfortunately — I do not have longterm follow-up of this case. The NSVT episodes and low ejection fraction are not unexpected given the diagnosis of a severe cardiac contusion in association with the diffuse ECG abnormalities seen in Figure-3.
• That said — the fact that this patient's condition seemingly stabilized and was continually improving after several days in intensive care bodes well for her potential recovery.

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Acknowledgment: My appreciation to Mehul K (from Delhi, India) for submission of today's case.

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ECG Blog #512 — Important Details ...

The ECG in Figure-1 was obtained from a middle-aged adult — who presented "acutely ill" with septicemia — but no chest pain.

• How would you interpret this ECG?
• Should you activate the cath lab? 
• If not — Why not?

Figure-1: The initial ECG in today's case — obtained from a middle-aged patient with septicemia, but no chest pain. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on this CASE:

The rhythm is sinus, at a rate just under 100/minute (ie, The R-R interval is just over 3 large boxes in duration). Intervals (PR,QRS,QTc) and the axis look normal. No chamber enlargement. 

Regarding Q-R-S-T Changes:

• Q Waves — are seen in each of the inferior leads. At least in lead III — the Q wave looks somewhat wider than is usually seen (which suggests this may be an "infarction Q wave" from an MI that occurred at some point in time).
• R Wave Progression — The R wave in lead V2 looks slightly taller than is generally seen in this lead. That said, the point for transition (ie, where the R wave becomes taller than the S wave is deep) — is normal (seen here to occur between lead V2-to-V3).

Regarding ST-T Wave Changes: 

• The 3 inferior leads (seen in Figure-2 within the RED rectangles) — each show slight-but-real ST elevation, with ST segment straightening in leads II and III.
• PEARL #1: Viewed in isolation — it would be difficult to know if the Q waves and slight-but-real ST elevation that we see in leads II,III,aVF indicate an acute (or recent) OMI, especially given the absence of CP (Chest Pain). But in the context of lead aVL (that manifests a nearly perfect, mirror-image opposite picture to what we see in lead III) — we have to at least consider a recent or acute event until proven otherwise (Note the slight ST depression with terminal T wave positivity seen within the BLUE rectangle in Figure-2). 
• KEY Point: As shown in ECG Blog #171 — Blog #158 and Blog #474 (among others) — one of the most helpful clues for determining whether subtle ST elevation in the inferior leads represents acute or recent OMI — is the presence of a mirror-image opposite ST-T wave picture between leads III and aVL. I find this reciprocal relationship almost "magical" in its reliability for suggesting an acute OMI (Occlusion-based Myocardial Infarction) based on the nearly opposite anatomical location in the frontal plane of lead III (at +120 degrees) and lead aVL (at -30 degrees). 

Figure-2: I've labeled key findings in the initial ECG.

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• NOTE #1: See my ADDENDUM below for review of the concept of what is an "OMI" (vs the outdated concept by clinicians "stuck" on insisting on STEMI criteria before they consider thrombolytic therapy or cath with PCI).
• NOTE #2: In today's case — Assessment as to whether STEMI criteria are met is difficult (ie, Seeing whether ≥1 mm of ST elevation is attained in at least 2 inferior leads). This is because there is PR segment depression in the inferior leads in Figure-2. Clinically, this should not matter — because what really counts is whether or not there is acute coronary occlusion — and PEARLS #1 and 2 suggest that an OMI is present regardless of whether or not STEMI criteria are satisfied!

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PEARL #2: Additional support regarding our concern for an ongoing acute inferior OMI — is forthcoming from the appearance of lead V2 (BLUE arrow in this lead in Figure-2).

• Because of the common blood supply in most patients between the inferior and posterior walls of the left ventricle — seeing a suggestion of acute posterior OMI adds support that uncertain limb lead findings are likely to be "real".
• This is precisely what we see in Figure-2. As is often emphasized in this ECG Blog — there normally is slight, upward sloping ST elevation in leads V2 and V3. However, the BLUE arrow in lead V2 highlights ST-T wave flattening with slight ST depression in this lead that is clearly abnormal.
• KEY Point: When inferior OMI is suspected — the presence of ST depression that is maximal in leads V2, V3 and/or V4 suggests associated posterior OMI. And, in today's case — it is this ST-T wave flattening and depression in lead V2 that tells us we have to consider the inferior lead ST elevation as recent until proven otherwise.
• 
  
• PEARL #3: In addition to suspected recent infero-postero OMI — there may also be RV involvement in Figure-2. This is because, rather than ST depression — the ST segment in lead V1 is coved and not at all depressed (as would be expected with a posterior OMI). 
• If there is simultaneous posterior OMI and acute RV involvement — then ST elevation in right-sided lead V1 from the RV MI may attenuate the amount of ST depression that we would otherwise see in lead V1 from posterior OMI. For this reason — an ECG with right-sided chest leads would ideally have been recorded as the best way to quickly determine if there is (or is not) RV involvement (See ECG Blog #190 for more on ECG recognition and management concerns regarding acute RV involvement).
• 
  
• PEARL #4: More than the ST-T wave flattening and depression that we see in lead V2 — the remaining leads in Figure-2 are also abnormal (ie, leads I; V3,V4,V5,V6 all manifest either ST-T wave flattening and/or a lack of clearly upright T waves). In the context of suspected recent or acute infero-postero OMI — these nonspecific ST-T wave findings suggest that in addition to the acute event, the patient may have significant underlying multi-vessel disease.

MY Clinical Impression: This is a difficult case — that is clearly complicated by the following: i) This patient is acutely ill with septicemia; — and, ii) The patient is not having chest pain! That said — my thoughts when this case was sent to me were the following:

• There most likely has been a recent infero-postero OMI. Whether this represents an ongoing acute event is impossible to determine from this single ECG without the benefit of additional clinical information (ie, a more complete history; comparison with a previous "baseline" ECG to see if the above-described ECG changes are "new"; serial Troponins; Echo at the bedside looking for a localized wall motion abnormality; etc.).
• Right-sided chest leads would have ideally been obtained to assess for the possibility of associated RV MI.
• Apart from any acute event — this patient may have multi-vessel disease with an unknown pattern of collateralization.
• Cardiac catheterization (sooner rather than later) may be needed to determine if an acute event is ongoing. That said — the timing for when to perform cardiac cath is complicated by the patient's other acute illness ( = septicemia). Ideally, at least some degree of stabilization would be achieved before beginning to contemplate acute intervention from this patient's presumed OMI. Admittedly — determining the optimal moment for intervention is a "juggling" act.

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The CASE Continues:

• The patient responded positively to initial treatment of his septicemia.
• Additional history was obtained — indicating that the patient did have chest pain prior to coming to the hospital!
• Initial Troponin was moderately elevated.
• As shown in Figure-3 — a repeat ECG was obtained. The patient's CP was "less" at the time of this repeat ECG.

QUESTIONS regarding Figure-3:

• How would you interpret the repeat ECG?
• Does Figure-3 confirm the diagnosis of an acute OMI?

Figure-3: Comparison between the 2 ECGs in today's case.

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MY Answers:

Clinically, the most useful way to interpret the repeat ECG shown at the bottom in Figure-3 — is to compare this tracing with today's initial ECG.

• First — Note how much easier it is compare serial ECGs when the 2 tracings you are looking at are placed side-by-side (as they are in Figure-3).
• My overall impression — is that the repeat ECG is clearly improved compared to the initial ECG that appears at the top of Figure-3.
• Of note — QRS amplitude is reduced in many leads in the repeat ECG. This is of uncertain significance. However, the frontal plane axis and R wave progression in the chest leads are similar in both tracings — such that lead-by-lead comparison should be valid.
• Accounting for the reduced QRS amplitude in ECG #2 — ST elevation is less in each of the inferior leads, and the reciprocal ST depression that had been seen in lead aVL (and to a lesser extent in lead I) on the initial ECG is no longer present. 
• In the chest leads — ST coving in lead V1 is less. 
• ST depression is no longer seen in lead V2, now with some return of a T wave in this lead.
• Lateral chest lead ST-T waves now look less abnormal.

BOTTOM Line:  The moderately elevated Troponin confirms infarction. Given reduction in the severity of this patient's CP in association with the above subtle-but-real improvement in ST-T wave appearance — I interpreted the repeat ECG in Figure-3 as suggestive of "dynamic" ST-T wave changes, providing further support of an evolving acute event.

• Cardiac catheterization was performed — and revealed severe triple-vessel disease!
• Unfortunately, I lack further details regarding follow-up.

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Final PEARL:

Figuring out what happened when with respect to acute coronary occlusion is challenging at best — and nearly impossible to do in the absence of timely documentation during the process.

• In my experience — correlation between the presence and relative severity of CP and the timing of each ECG obtained — can rarely be determined by retrospective review of the patient's chart.
• That said — Wouldn't it be EASY to document this correlation between CP severity with each serial ECG if this was done at the time that the patient is being evaluated in the ED? (ie, Medical providers can simply write ON each actual ECG [as well as in the chart] the severity of CP at the time each ECG is recorded).
• Doing so would then give us a "story" — that we can then piece together into the most reasonable clinical scenario (that should tell us if the "culprit" vessel is open or closed at the time of each tracing).
• Doing so would also clue us into the "pseudo-normalization" period that may occur following spontaneous reperfusion with reduction in CP (ie, No more than minimal if any ECG abnormalities may be seen if the initial tracing occurs in between the period of ST elevation on the way to reperfusion T wave inversion).
• For example, in today's case — knowing that the patient's CP had decreased in association with the timing of the repeat ECG allowed us to appreciate that relatively modest improvements in ECG findings are consistent with "dynamic" ST-T wave changes.

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Acknowledgment: My appreciation for the anonymous submission of today's case.

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ADDENDUM (1/3/2026): 

For more regarding the concept and ECG interpretation of OMIs (that do not satisfy millimeter-based STEMI criteria):

• Check out ECG Blog #337 — that reviews a case with focus on distinction between a "NSTEMI" vs an OMI.
• Consider the 2 Audio Pearls at the bottom of this page.
• Consider Figure-4 — which reviews some ECG findings to look for when you suspect an acute OMI in a patient who does not satisfy the millimeter-based STEMI criteria that I review below this Figure.

Figure-4: ECG findings to look for when your patient with new-onset cardiac symptoms does not manifest STEMI-criteria ST elevation on ECG.
= = = = =
KEY Note #1: Insistence in satisfying millimeter-based STEMI criteria before considering prompt cath with PCI (or thrombolytic therapy when access to 24/7 cath-capability is not available) — will miss at least 1/3 of all acute coronary occlusions. In a patient with new CP — attention to the ECG findings in Figure-4 may allow you to identify these patients with an acute OMI despite lacking STEMI criteria.
= = = = =
KEY Note #2: Loss of potentially viable myocardium is actually much greater than that implied in Note #1 — because even for patients in whom a "STEMI" is eventually recognized — by waiting until millimeter-based criteria are finally satisfied, the needed reperfusion therapy (PCI or thrombolytic therapy) is all-too-often delayed (often by many hours!). Time is critical! — as the greatest amount of potential myocardial-saving benefit occurs when reperfusion therapy is provided within the first few hours! (with the self-fulfilling prophecy that the outdated and inferior "STEMI-paradigm" gets perpetuated in the literature — because data will be recorded saying PCI was delivered "within minutes" of STEMI elevation [neglecting the clinical reality that OMI-criteria will often have been present hours earlier! ] ).
= = = = =
Note #3: See ECG Blog #318 — for clarification of T-QRS-D (Terminal QRS Distortion = my 2nd bullet in Figure-4).

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How a "STEMI" is Defined:

I've excerpted the following Akbar and Mountfort's citation in StatPearls, 2024 — of ECG Guidelines for defining a "STEMI" from the AHA (American Heart Association), ACC (American College of Cardiology), ESC (European Society of Cardiology), and the WHF (World Heart Federation):

• New ST-segment elevation of ≥1 mm at the J point in 2 contiguous leads (except in leads V2 and V3).
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• In leads V2 and V3:
• ST elevation ≥2 mm for men >40 years of age.
• ST elevation ≥2.5 for men ≤40 years of age.
• ST elevation ≥1.5 mm for women.

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—  —

ECG Media PEARL #10 (10 minutes Audio) — reviews the concept of why the term “OMI” ( = Occlusion-based MI) should replace the more familiar term STEMI — and, reviews the basics on how to predict the "culprit" artery.

—  —

ECG Media PEARL #11 (6 minutes Audio) — Reviews how to tell IF the “culprit” (ie, acutely occluded) artery has reperfused, using clinical and ECG criteria.