EXTRA-MAGNUS- Why the Sudden Shock after a Few Days of Malaise? -SSmith (9-5-2024)

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Written by Magnus Nossen - Edits by Grauer and Smith

The patient in today’s case is a woman in her 70s with a previous medical history of HTN and hyperlipidemia. She presented to an outside hospital after several days of malaise and feeling unwell. At the time of admission, her vital signs were normal. Heart rate was in the 80s. She had a very elevated troponin T at 12,335 ng/L at the time of presentation. (This is a value typical for a large subacute MI, normal value < 0-14ng/L.)  

Below is the presentation ECG.

The patient initially denied chest pain, but when questioned directly — did admit to vague "chest discomfort" in previous days. She was transferred to our facility for angiography. On arrival she was without distress. Due to acute renal failure and the duration of her symptoms over a number of days — it was decided to perform angiography the following day. Serial Troponin T values were decreasing, consistent with subacute completed MI. The ECG on admission showed sinus rhythm with a heart rate in the 80s — and was consistent with a subacute completed inferior, lateral and posterior transmural infarction, with Q waves and ST elevation in the inferiolateral leads — and ST depression in lead V2. The patient was put on telemetry while waiting for angiography the following day.

The patient awoke suddenly during the night — stating that she felt "strange". The ECG below was recorded at this time. What do you think?

This ECG is consistent with infero-postero-lateral infarction — with persistent inferior lead ST elevation and reciprocal high-lateral ST depression — ST depression in lead V2 — and some terminal T wave inversion in inferior and lateral chest leads. It is not significantly different from the admission ECG. Perhaps the most remarkable change — is the increase in heart rate, with this ECG now showing sinus tachycardia at 118/minute! Also of note is the still upright (not inverted) T waves. Persistent ST elevation with upright T waves >48 hours after myocardial infarction is associated with Post-Infarction Regional Pericarditis (PIRP).

Sinus tachycardia has many potential causes. In my experience, for the patient at rest and not anxious — it often signifies severe illness. This is especially true for the elderly patient with sinus tachycardia. The patient in today’s case suddenly became tachycardic while sleeping. The heart rate almost doubled within a minute. What might account for the sudden rate change in this patient? See if you can identify the problem in the below parasternal view of the heart.

The above video file was recorded from a subcostal «window» and it shows the heart with all four chambers. Right atrium, right ventricle, left atrium and left ventricle viewed through the liver. What is the cause of the sudden tachycardia? 

Below is a still image from the above video. The heart chambers are annotated. From the subcostal "window" the heart is viewed through the liver and thus the liver parenchyma is closest to the transducer (top of the image). Below the liver is the heart with the right atrium (RA), right ventricle (RV), left atrium (LA) and left ventricle (LV) The red arrow points to a large opening in the basal region of the interventricular septum. This is a ventricular septal rupture (VSR). As already mentioned, this patient could have post-infarction regional pericarditis from a large completed MI. PIRP is strongly associated with myocardial rupture. This patient developed a rupture of the basal portion of the interventricular septum (VSR). The VSR is what is causing the cardiogenic shock!

A Short Comment on PIRP and T Waves: 

Oliva et al found a strong association of myocardial rupture with postinfarction regional pericarditis. PIRP was associated with persistent upright T waves. He found two types of atypical T wave development in PRIP

1) Persistently positive (upright) T waves beyond 48 hours in a patient with acute MI

2) Premature change from inverted T waves to pseudonormal T waves (within 48-72 hours) 

In our case, PIRP is a likely explanation for the continued positive T waves. Since serial ECGs are not available so either of the two patterns described above could be present (only serial ECG could differentiate). 

Another possible cause of pseudonormalization of T waves mentioned many times on this blog is the pseudonormalization caused by re-occlusion of an infarct related reperfused coronary artery. This does not fit with the clinical scenario in today's case. 

Below are two more video files. These images were obtained  from the parasternal short axis which transects the left and right ventricles. The VSR is located in inferior and basal portion of the ventricular septum and is readily visible. The second video file below shows the shunt by color doppler. 

Discussion: The patient in today’s case experienced a mechanical complication secondary to completed OMI. Troponin at presentation was very significantly elevated and T waves were still upright. She had atypical symptoms which made her postpone seeking medical attention. Mechanical complications secondary to myocardial infarction are infrequent due to most patients receiving revascularization quite rapidly. The patient in today’s case developed a large basal septal ventricular septal rupture (VSR) as a complication of an untreated OMI. Auscultation of a NEW harsh holosystolic murmur lead to rapid evaluation with echocardiography that confirmed the clinical suspicion. 

A VSR will lead to sudden left to right shunt and if large enough can lead to low output left sided failure. The RV acts as a conduit and does not necessarily become acutely dilated. Left ventricular afterload reduction is essential to decrease the trans-septal pressure gradient and thus decrease shunt volume, making a larger proportion of the blood flow from the left ventricle through the aortic valve.

For the patient in today's case nitroprusside (vasodilator) infusion was started to lower systemic vascular resistance (SVR), and an intra aortic balloon pump (IABP) was placed to further decrease afterload and better the hemodynamics. Surgical repair of the VSR was eventually done. The patient needed short term dialysis post surgery, but she eventually made a full recovery.

Mechanical complications are dreaded sequela of myocardia infarctions and can  come in the form of free wall rupture, ventricular septal rupture or papillary muscle rupture. The true incidence of the three mechanical complications may differ from reported incidence due to underreporting, miscoding, or variation in the populations studied. It has been estimated that in the aggregate, they occur at a rate of about 3 per 1000 patients with acute MI, and most of these events occur in patients with STEMI. Among patients with STEMI, ventricular septal rupture is the most common and free wall rupture is the least common. 

Mechanical complications occur acutely and significantly alter hemodynamics leading to compensatory mechanism which usually involve vasoconstriction and tachycardia, both hallmarks of cardiogenic shock. 

A VSR is more likely to occur in patients who are older, female, hypertensive, have chronic kidney disease, and have no prior history of smoking. It commonly occurs in the setting of a first myocardial infarction (MI) in the background of delayed or absent reperfusion therapy. Angiography usually reveals an absence of collateral circulation to the infarct zone. 

Because previous ischemia induces myocardial preconditioning, decreasing the likelihood of transmural myocardial necrosis and myocardial rupture, patients with evidence of diabetes mellitus, chronic angina or previous MI are less likely to experience a rupture. VSR may develop within 1-14 days post MI, however it’s incidence usually shows a bimodal peak which is within 24 hours and after 3-5  days post MI.

Survival after ventricular septal rupture may occur only after surgical repair. Thus, the diagnosis of ventricular septal rupture should prompt a heart team discussion of options. This discussion should take into account that, for some patients, surgery is futile as mortality approaches 100 percent. Older patients and those with poor right ventricular function often fall into this group. The timing of ventricular septal rupture repair is controversial.

Subacute AnteroSeptal STEMI, With Persistent ST elevation and Upright T-waves

Learning Points:

1. Sinus tachycardia (especially in the elderly) often signifies serious illness as it did in today’s case.
2. Mechanical complications of transmural infarction are rare and dreaded sequela and have high morbidity and mortality. 
3. Post infarction regional pericarditis (PIRP) can be suspected from the ECG and is associated with an increased risk of myocardial rupture.

Oliva PB, Hammill SC, Edwards WD. Electrocardiographic diagnosis of postinfarction regional pericarditis

Oliva PB.  Hammill SC.  Edwards WD.  Cardiac rupture: a clinically predictable complication of acute myocardial infarction

Ventricular septal rupture

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MY Comment, by KEN GRAUER, MD (9/5/2024):

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As I emphasized in My Comment in the December 6, 2022 post and the August 19, 2023 post of Dr. Smith's ECG Blog — Not all patients with acute MI report chest pain. I thought the presentation of today's case makes it worthwhile to review the data regarding this issue.

• As per Dr. Nossen — today's patient concerns an older woman with a several day history of malaise and "not feeling well". Mention of vague "chest discomfort" over a period of recent days was only elicited when specifically requestioned. By history — providers were not expecting her initial ECG to show recent completed infarction with marked Troponin elevation.

The Framingham studies from many years ago taught us that the incidence of “Silent MI” is as high as ~30% of all MIs (Kannel & Abbott: N Engl J Med 311(18):1144-1147, 1984 — Kannel: Cardiol Clin 4(4):583-591, 1986).

• The interesting part of this data is that in about half of this 30% (ie, ~15% of all patients with MI) — patients found on yearly follow-up ECGs to manifest clear evidence of infarction had NO symptoms at all — therefore truly “silent” MIs.
• But in the other half of this 30% (ie, in ~15% of all patients with MI) — although these patients found on follow-up ECG to have had infarction did not have chest pain — they did have "something else" thought to be associated with their MI.
• The most common “something else” symptom was shortness of breath. Other non-chest-pain equivalent symptoms included — abdominal pain — “flu-like” symptoms (ie, myalgias; not “feeling” good) — excessive fatigue — syncope — mental status changes (ie, as might be found in an elderly patient wandering from home).
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• BOTTOM Line: It's especially important for emergency providers to be aware of the entity of “Silent MI” — which can either be completely “silent” — or, associated with a non-chest-pain equivalent symptom. The incidence of both types of silent MI is more common than is often appreciated. Not all patients with acute (or recent) MI have chest pain with their event.

Application to Today's Case: Today's patient developed ventricular septal rupture the evening after she was admitted to the hospital. Her nonspecific symptoms that brought her to the hospital began a number of days before she finally sought medical assistance. 

• Awareness that this patient's malaise and her "not feeling well", as well as her vague chest discomfort might represent a cardiac problem — could have resulted in more timely initiation of treatment, that potentially might have averted the severe mechanical complication of her initially unrecognized extensive infarction.

  

EXTRA COPY — ECG Blog #516 — The Patient is Post-Op - EXTRA COPY

The ECG in Figure-1 was sent to me — with the only history provided being "that this ECG was recorded following an operation". The nature of the surgery is unknown.

QUESTIONS:

• How would YOU interpret the ECG in Figure-1 ?
• Is this history helpful for making the diagnosis?

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

ANSWERS:

When presented with a 12-lead ECG and a long lead rhythm strip — I favor taking an initial brief look at the rhythm strip before I look at the 12-lead tracing. In the space of a few seconds — I hope to find out the following:

• #1) Does the rhythm need immediate treatment? (as might be the case if the rhythm was excessively fast or slow).
• #2) IF the patient is hemodynamically stable and the rhythm does not need immediate treatment — I then take a brief look at the rest of the 12-lead ECG.

With regard to Rhythm Assessment — I favor time-efficient use of the Ps, Qs, 3R Approach (as described on ECG Blog #185). I like to begin with whichever of the 5 KEY Parameters is easiest to assess.

• The QRS in Figure-1 is obviously wide (clearly more than half a large box in duration).
• The ventricular rhythm is almost (but not completely) Regular — in that R-R intervals vary between being a little more or a little less than 5 large boxes in duration.
• The Rate of the rhythm is ~60/minute (300 ÷5 ~60/minute).
• Some P waves are present! That said — we do not see P waves throughout the entire tracing.
• The P waves that we do see do not appear to be Related to neighboring QRS complexes (because the PR interval looks to be continually changing).

MY Initial Brief Impression: The presence of a fairly regular, wide QRS rhythm — and the lack of relationship between P waves and neighboring QRS complexes suggest a significant degree of AV block (probable 2nd- or 3rd-degree AV block).

• We do not yet know about this patient's hemodynamic status. That said — a wide QRS rhythm at a rate of ~60/minute (even if this represents 2nd- or 3rd-degree AV block) — usually does not need immediate treatment.
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• PEARL #1: Whenever we detect that the QRS is wide — we want to determine as quickly as possible WHY is the QRS wide?
• Is QRS widening the result of some form of bundle branch block?
•   — OR — Is this a ventricular rhythm?

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QUESTION:

• Why did YOU think the QRS is wide in Figure-1?

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ANSWER: 

There are a limited number of possible answers to this question. These possible answers include:

• #1) There is a supraventricular rhythm with some type of conduction disturbance. As reviewed in ECG Blog #204 — there are 3 basic types of conduction disturbances ( = RBBB, LBBB and IVCD).
• #2) There is WPW.
• #3) There is a ventricular rhythm.
• #4) There is some type of "toxicity" causing QRS widening.

Regarding these possible answers:

• WPW is not present — as P waves are not conducted, and there are no delta waves.
• QRS morphology does not resemble any known form of conduction disturbance (ie, There is no upright QRS in lead V1, as would be the case with RBBB — and the QRS is essentially all negative in all 3 inferior leads and in all 6 chest leads). This strongly suggest a ventricular rhythm.

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At this point — I took a closer look at QRST morphology in the 12-lead ECG.

• QUESTION: Did YOU notice peaking of T waves?

ANSWER:

• ST-T waves look overly peaked (if not pointed) in multiple leads (ie, in leads II,III,aVF; and V3-thru-V6). The size of many of these T waves looks to be disproportionately increased with respect to the size of S waves in these leads.
• This patient almost certainly has significant Hyperkalemia — so much so, that I'd empirically give IV Calcium, even before knowing what the serum K+ level is.

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KEY Points about Today's CASE:

Unfortunately I lack information regarding the specifics of follow-up in today's case. Nevertheless, I thought it important to point out an example in which empiric use of IV Calcium is appropriate even before we know the laboratory value of serum K+.

• My discussion of a similar case in ECG Blog #275 reviews the textbook description for sequential ECG changes seen with progressive degrees of hyperkalemia. But many patients do not read the textbook — such that any sequence of ECG changes may be seen (including cardiac arrest prior to T wave peaking and QRS widening).

PEARL #2: The brief history that we were provided with (namely that today's ECG was recorded from a post-op patient) — is relevant because there are many potential causes of hyperkalemia in the post-operative state (Ayach et al — Eur J Intern Med 26(2):106-111, 2015) - and - (Jung et al — Acute and Crit Care 33(4):271-275, 2018) - and - (Dixit et al — Ann Cardiac Anaesth 22(2):162-168, 2019). These potential precipitating causes of hyperkalemia in the post-operative state may include the following:

• Increased K+ release from cells as a result injury sustained during surgery.
• Reduced urine output/acute renal insufficiency.
• Hypovolemia (that may have been present before surgery — or developed during surgery).
• Exogenous K+ load (ie, from blood transfusions).
• Rhabdomyolysis (from malpositioning of the patient during surgery).
• Use of K+-retaining medications just before or during surgery.
• Acidosis (which promotes redistribution of K+ from intracellular to extracellular compartments).

PEARL #3: Rapid recognition of Hyperkalemia is among the most important of skills for emergency providers to master. The reasons for this are simple: 

• i) Hyperkalemia is potentially life-threatening.
• ii) There is an empiric treatment (ie, IV Calcium) that can be life-saving — and which should sometimes be given prior to lab confirmation of hyperkalemia. Cautious administration of IV Calcium is safe — and, not-to-promptly treat the patient risks losing the patient.
• iii) Not-to-recognize hyperkalemia as the cause of QRS widening, unusual rhythm disturbances and/or ST-T wave abnormalities — will lead you down the path of potentially serious misdiagnosis.

 

PEARL #4: Considerations regarding use of IV Calcium:

• IV Calcium works fast (ie, within 2-3 minutes) by an action that stabilizes myocardial membrane potential, thereby reducing cardiac membrane excitability provoked by hyperkalemia (and thereby protecting against cardiac arrhythmias). NOTE: IV Calcium does not cause intracellular potassium shift, and it does not facilitate elimination of this cation.
• Either Calcium Chloride or Calcium Gluconate can be used (10 mL given IV over 3-5 minutes with ECG monitoring). NOTE: The chloride form contains 3X the amount of calcium per 10 mL dose (10 ml 10% CaCl = 6.8 mmol Ca++ vs 10 ml 10% CaGlu = 2.3 mmol Ca++). 
• IV Calcium should be repeated IF there is no effect (ie, narrowing of the QRS on ECG) after 5-10 minutes. More of the gluconate form may need to be given (since it contains less calcium). 
• The duration of action of IV Calcium is only ~30-60 minutes — but this is more than enough time to allow other  treatments to work.
• CaGlu can be given through a peripheral IV line. Because CaCl is more likely to cause tissue necrosis if there is extravasation — a central line is recommended (except if your patient is in cardiac arrest). 
• Other treatments will often be needed (ie, Glucose/Insulin; Albuterol inhalation; Sodium Bicarbonate — and in refractory cases, hemodialysis) — but IV Calcium is the initial treatment of choice for life-threatening hyperkalemia.
• NOTE: IV Calcium is not indicated for the treatment of peaked T waves with a narrow QRS and reasonable rhythm — as this is not a life-threatening situation.

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PEARL #5: Assessment of the rhythm with severe hyperkalemia is often difficult for several reasons (as summarized below in Figure-2): 

• As serum K+ goes up — P wave amplitude decreases. Eventually — P waves disappear.
• As serum K+ goes up — the QRS widens.
• In addition to bradycardia — any form of AV block may develop. Therefore — Think of hyperkalemia in the presence of any bradycardia when the QRS is wide (even if there is no T wave peaking).
• Cardiac arrhythmias that develop in association with severe hyperkalemia often "do not obey the rules" — such that identification of a specific rhythm diagnosis may not be possible in patients with severe hyperkalemia.

THINK for a MOMENT what the ECG will look like IF you can't clearly see P waves (or can't see P waves at all) — and the QRS is wide?

• ANSWER: The ECG will look like there is a ventricular escape rhythm — or — like the rhythm is VT if the heart rate is fast.

 

PEARL #6: As we have just noted, with progressive hyperkalemia — P wave amplitude decreases until ultimately P waves disappear. 

• Interestingly — the sinus node is often still able to transmit the electrical impulse to the ventricles in such cases, even though no P wave may be seen on ECG. This is known as a sinoventricular rhythm.

 

Figure-2: Why assessing the rhythm with hyperkalemia is difficult.

PEARL #7: In my opinion, it is not worth wasting time trying to figure out the specific rhythm diagnosis of a bradycardia when there is hyperkalemia. I used to spend hours trying to do this — but after years of doing so, I finally realized the following: 

• i) That a specific rhythm diagnosis may not be possible when there is significant hyperkalemia — and, even if you succeed in making a diagnosis such as Wenckebach — chances are as serum K+ intra/extracellular fluxes change, that the cardiac rhythm will also soon change; and, 
• ii) Clinically — it does not matter what the specific rhythm diagnosis is once you recognize hyperkalemia that needs to be immediately treated — because usually within minutes after giving IV calcium, the "bad" rhythm will probably "go away" (often with surprisingly rapid reestablishment of sinus rhythm).

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What about the Rhythm in Today's CASE?

Let's return to today's ECG. We determined in Figure-1 (that I reproduce below) — that the rhythm is fairly (but not completely) regular, at an average rate of ~60/minute — with some P waves that do not appear to be related to neighboring QRS complexes.

• KEY Point: QRS morphology in Figure-1 does not resemble any known form of conduction defect (ie, the all-negative QRS across the 6 chest leads suggests that the wide QRS represents a ventricular rhythm).

QUESTION:

• Are there additional P waves that are hidden in Figure-1?

Figure-1: I've reproduced the initial ECG in today's case.

PEARL #8: The BEST way to look for additional P waves that may be partially (or completely) hidden — is to find 2 or more definite P waves that occur in a row (ie, the 2nd and 3rd — and then the 4th and 5th RED arrows in Figure-3). 

• Set your calipers to this P-P interval suggested by the distance between 2 consecutive RED arrows. 
• Note in Figure-3 — the partially hidden PINK arrow P wave that precedes the 4th and 5th RED arrow P waves. These last 3 colored arrows suggest what the P-P interval might be for a fairly (but not completely) regular underlying sinus rhythm.

Figure-3: I've identified those P waves that we definitely see ( = the RED arrows). To this, I've added a PINK arrow for what appears to be a partially hidden P wave.

Following through with the P-P interval suggested by consecutive RED arrows in Figure-3 — I've added WHITE arrows in Figure-4 to highlight where I suspect additional sinus P waves may be hiding.

Figure-4: Colored arrows suggest an underlying sinus arrhythmia.

NOTE: Assuming the colored arrows in Figure-4 indicate where sinus P waves lie — it would appear that today's rhythm is probably complete AV block.

• That said, when AV block is truly "complete" — the ventricular escape rhythm tends to be more regular than what we see in Figure-4. Most of the time — QRS complexes that appear earlier-than-expected are the result of some conduction (therefore 2nd-degree instead of 3rd-degree AV block).
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• BOTTOM Line: None of this matters clinically! It is simply not worth wasting time trying to distinguish between 2nd-degree vs 3rd-degree AV block in Figure-4 — because arrhythmias often "do not obey the rules" when there is significant hyperkalemia — and the rhythm will probably normalize within minutes of giving IV Calcium.

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Acknowledgment: My appreciation to Ahmed Marai, Safen Haider, and Zahraa Ali (from Iraq) — for allowing me to use this case and these tracings.

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ADDENDUM (XX/XX/2026):

—  —

ECG Media PEARL #58 (8:30 minutes Audio) — Reviews some lesser-known Pearls for ECG recognition of Hyperkalemia.

 

EXTRA COPY- ECG Blog #514 — ST Elevation from Pericarditis-EXTRA COPY

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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?
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• 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:

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Figure-4: XXXX

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THE CASE:

Ahmed Adel — FB Messenger (11/23/2025)

— Await permission from Ahmed (from Baghdad, Iraq) —

 

AHMED — Please feel free to use the case for your blog. It would mean a lot, and I'm excited to read it! 

Yes, it's Ahmed Adel from Baghdad, Iraq.

 

Yes, that clears everything up. 

Thank you so much, Dr. Ken. I really appreciate you taking the time to review the case & share your insights.

 

ME— THANKS Ahmed. I may be a month or so until I get to it, as I have other cases before — but I think it is a very important case! — :)

THE CASE:

Hello Dr. Ken, hope you’re doing well. I wanted to share this interesting and educational case with you, and I’d really appreciate any insights you might have whenever you have the time.

 

A 55-year-old male with a negative past medical history presented with chest pain.

 

The senior cardiologist diagnosed this as pericarditis based on the diffuse concave ST elevations and the “PR depression with a Spodick sign in lead II.” He wanted to start the patient on an NSAID & colchicine.

 

But my colleague who recieved this patient in the ED wasn't convinced & called me for a second opinion regarding this case. My opinion was: "lead II is entirely slanted (wandering baseline) giving the FALSE appearance of PR depression & Spodick sign. V3 shows terminal QRS distortion (TQRSD), which is a HUGE RED FLAG for a potential LAD occlusion. I think it would be wise to withhold the NSAID for now & order serial ECCs & trops before calling this a pericarditis".

 

Shortly after, the patient went into VFib & shocked back into sinus rhythm... twice!

 

A repeat ECG showed dynamic changes with a new ST depression in lead II, which I think confirms LAD (wraparound?) occlusion.

 

 

 

I have a few questions:

• Would you have activated the cath lab based on clinical suspicion + the initial ECG (which only had TQRSD in V3 as the only clue for OMI that I could find)?

• Were there any other "red flags" in the initial ECG that were missed?

• Do you know of any literature on the value of TQRSD in differentiating LADO from pericarditis? I only know of its use in LADO vs BER. Thank you in advance!

 

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MY REPLY:

Hello Ahmed. I completely agree with you!

I would like to use this case for an ECG Blog — because it is indeed challenging, with the very important lesson of calling this an acute STEMI (not just an "OMI" — but there is enough ST elev. to call this a STEMI)-in progress until proven otherwise.

 

I'd be happy to acknowledge you if you like (Is it Ahmed Adel from Baghdad, Irag? ) — or if this case is too "sensitive" — I could make it anonymous. Just let me know if you would allow me to write this case up — :)

 

So — Statistically, it's important to remember that in a patient with new CP (Chest Pain) — acute MI is much, much more common than acute pericarditis — which is why Dr. Smith says, "You diagnose acute pericarditis at your peril!"

 

There clearly are features that could be consistent with acute pericarditis = diffuse ST elevation — and a positive ST-T wave ratio in lead V6 (See my ECG Blog #365 and my ECG Blog #208). But #1) There is NO mention of the nature of CP (pleuritic? positional? as it should be with pericaridits) — lead II looks more like lead III (should be that lead II looks more like lead I with pericarditis) — and there is T-QRS-D in the 4 leads that I have circled (See my ECG Blog #318). So this ECG is unique in that I don't know that I've seen a case in which it is mainly the T-QRS-D that removed my doubt about an acute MI!

 

As to PR interval depression — I think it probably is seen in leads II, aVF, V3,4,5 — with some PR elevation in aVR — BUT — in my experience, PR depression is NOT a specific sign (I've seen this in normal ECGs and in acute MI).

 

As to Spodick's Sign — I sometimes think that ony Dr. Spodick can reliably identify this. It does look like Spodick's Sign may be present in V3-thru-V6 ... but I find the reproducibility of this sign by anyone other than Dr. Spodick (who is a true pericarditis expert) is very poor — so I never depend on Spodick's sign.

 

Finally, very subtle — is what looks like reciprocal ST dep in aVL (which does not occur with acute pericarditis!).

 

So YES — this ECG should have been repeated within 15 minutes and at the very least, one should have gotten Troponin to help.

 

I hope the above answers your questions. Your concerns are perfectly valid!

 

https://ecg-interpretation.blogspot.com/2023/02/ecg-blog-365-30yo-with-pericarditis.html

 

https://ecg-interpretation.blogspot.com/2021/03/ecg-blog-208-ecg-mp-25-st-elevation-but.html

 

 

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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).