ECG Blog #516 — The Patient is Post-Op ...

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 the next 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: As noted above — the QRS complex is wide. 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 the above question. These possibilities include:

• #1) There is a supraventricular rhythm with some type of conduction disturbance (due to either aberrant conduction or preexisting bundle branch block). 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.
• Aberrant conduction is most often seen in association with a rapid ventricular rate — and the heart rate here is not fast.
• 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 suggests 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.
• My Impression: This patient is almost certain to have 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 of 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 most 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 at least some P waves, albeit these P waves 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 (1/31/2026):

—  —

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

 

ECG Blog #515 — Who is the "Culprit?"

The ECG in Figure-1 is from a 67-year old man who presented with new CP (Chest Pain).

• How would YOU interpret this ECG? 

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

NOTE: The KEY question relates as to whether the ST-T wave changes are the result of the rhythm? — vs whether they represent an acute MI? (or both?).

• This case is presented by Dawn Altman in her ECG Guru (The case contributed by Natalie Terrana).
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• CLICK HERE — for my detailed discussion. (Scroll up on the ECG Guru page to see Dawn's detailed presentation).

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.
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• 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!
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• 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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