ECG Blog #517 — Recurrent Syncope ...

The ECG in Figure-1 was obtained from an older woman who presented to the ED (Emergency Department) after suddenly waking up from sleep dyspneic, dizzy, and convinced she was "about to die".

QUESTIONS:

• How would YOU interpret her initial ECG shown in Figure-1?
• What do you think is the cause of her symptoms?

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

CASE Follow-Up:

Over the next few weeks — this patient was again seen in the ED on 2 occasions.

• On her 2nd-ED-Visit — She presented after syncope and a fall. She reported several episodes of "dizziness" in the days prior to this 2nd ED visit.
• Her exam in the ED was "normal".
• Her repeat 12-lead ECG was virtually identical to that seen in Figure-1.
• Basic lab was unremarkable.
• The patient was discharged home.

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• On her 3rd-ED-Visit — She presented to the ED with a presyncopal episode and ongoing dizziness.
• Her initial exam was unremarkable.
• Her repeat 12-lead ECG was once again unchanged from that seen in Figure-1.
• Basic lab was again unremarkable.
• The patient was placed on a monitor for a period of observation in the ED. Suddenly — the patient became unresponsive! The rhythm strip shown in Figure-2 was recorded.

QUESTIONS:

Realizing that Figure-2 is limited to a brief, single lead rhythm strip ...

• How would you interpret the rhythm in Figure 2?
• What diagnosis is suggested by the history in today's case — given the 2 tracings shown in Figures-1 and -2?

Figure-2: Brief telemetry recording on the patient's 3rd ED visit (normal 25 mm/sec calibration).

ANSWER:

The rhythm in Figure-2 shows marked bradycardia (21 large boxes = 4.2 seconds separate the 2 beats in the middle of the rhythm strip). The tracing ends with nearly 4 seconds of asystole (We don't know if another QRS complex ever occurred).

• It looks like very low amplitude but almost regular P waves are seen throughout the tracing

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COMMENT:

This sequence of events should not have happened. In Figure-3 — I've labeled the initial tracing to illustrate the ECG diagnosis that could have been made at the time of this patient's 1st ED visit.

• The rhythm is sinus at ~80-85/minute.
• The PR interval is at the upper limit of normal ( = 0.21 second).
• The QRS is wide (3 little boxes in duration = 0.12 second).
• QRS morphology in the chest leads is consistent with RBBB conduction (ie, predominant R wave in right-sided lead V1 — with a wide terminal S wave in lead V6).
• QRS morphology in the limb leads is consistent with LBBB conduction (ie, all upright QRS in left-sided leads I and aVL). In addition — there is marked LAD (Left Axis Deviation).

BOTTOM Line: The ECG in Figure-3 is consistent with MBBB (Masquerading Bundle Branch Block).

Figure-3: I've labeled today's initial ECG.

PEARL #1: ECG criteria for the diagnosis of MBBB are described by Dhanse et al (J Clin Diag Research: 10(9), 2016) — and Buttner and Cadogan (LITFL, 2021) — and include the following: 

• An ECG pattern consistent with RBBB in the chest leads (ie, with a widened, predominantly positive QRS in lead V1).
• An ECG pattern consistent with LBBB in the limb leads (ie, with a widened, monophasic QRS in leads I and aVL).
• 
  
• NOTE: Variations on this above "theme" of MBBB are common. Thus, the S wave that is typically associated with RBBB patterns in lateral chest leads V5,V6 may or may not be present. In the limb leads, rather than a strict LBBB pattern — more of an extreme LAHB (Left Anterior HemiBlock) pattern will often be seen (ie, with wide and predominantly [if not totally] negative QRS complexes in the inferior leads — and with a smaller [blunted] terminal s wave in leads I and aVL).
• 
  
• BOTTOM Line: Knowing the clinical history may aid in recognition of IVCD patterns that are consistent with MBBB (ie, if the patient has a known history of severe, underlying heart disease). Distinction from simple bifascicular block (ie, with RBBB/LAHB) — may be facilitated by seeing one or more of the following: i) More of a monomorphic upright QRS in lead V1 (which lacks the neatly defined, triphasic rsR' with taller right "rabbit ear" seen with typical RBBB); ii) Lack of a wide terminal S wave in lateral chest lead V6; iii) Seeing an all-positive (or at least predominantly positive) widened QRS in leads I and/or aVL, with no more than a tiny, narrow s wave in these leads; and/or, iv) Seeing widened, all-negative (or almost all-negative) QRS complexes in the inferior leads.

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Retrospective Reflection on Today's CASE:

Hindsight is 100% in the "retrospectoscope". That said — I think it instructive to reflect back on events in today's case.

• Given the history — one might not have chosen to insert a permanent pacemaker after this patient's 1st ED visit. However, the diagnosis of MBBB should be recognized from this initial ECG shown above in Figure-1 because the rhythm is sinus — the QRS is wide — and as shown in Figure-2, QRS morphology "looks" like RBBB conduction in the chest leads, but LBBB conduction with left axis in the limb leads.
• IF one recognizes MBBB on this 1st ED visit — and then considers the feeling this patient had on awakening "that she was going to die" — the astute clinician could have suspected that the patient may have had a bradyarrhythmic form of AV block, and therefore continued to monitor the patient in the ED (and depending on the history — potentially admitted the patient to the hospital for an additional 24 hours to monitor her rhythm).
• And, even if nothing showed on those additional 24 hours of telemetry, given the diagnosis of MBBB — the patient should have been warned to promptly report any "dizzy episodes". Especially given several subsequent "dizzy episodes" over the next few weeks, had this been done — the patient could have been diagnosed and paced long before her 3rd ED visit. 
• PEARL #2: As per the famous aphorism by Sir William Osler, "Listen to your patient; He/she is telling you the diagnosis". All too often the diagnosis is there being told to us by our patient, if we only allow ourselves to listen (ie, Today's patient telling us she was awakened with the feeling she was "about to die" — and then had more episodes of "dizziness" in the days prior to her 2nd ED visit).
• PEARL #3: The entity of MBBB is often cited in the literature as being "rare". That said, since I've become aware of this entity — in my experience, it is not rare. Instead, I find this situation similar to what I've experienced with certain specific ECG patterns, such as a Brugada-1 ECG, Takotsubo Cardiomyopathy — and blocked PACs. Each of these entities once seemed "rare" to me — until I became aware of them. And now that I've become experienced in recognizing Brugada-1 ECGs, Takotsubo CM, and blocked PACs — they are no longer "rare", but deceptively common under the right clinical circumstances (See ECG Blog #394 and Blog #419 for 2 more examples of MBBB).

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Is the QRS in today's ECG truly wide?

It's worth spending a moment reviewing the question as to whether the QRS complex in today's initial ECG is truly wide? After all, the QRS doesn't look that wide — Does it?

• Many textbooks describe QRS widening as being defined by a QRS ≥0.12 second in duration. But is this truly the best defining limit for QRS widening when there are cases of fascicular VT in which QRS duration is less than 0.12 second? (Kapa et al — Circ: Arrhythm and Electrophys 10(1), 2017).
• The definition of QRS widening is different in children. The reason for this is simple: It takes less time to depolarize a smaller heart. Therefore, QRS duration should normally be ≤0.10 second in children up to ~12 years of age (Rijnbeek et al — Eur Heart J 22:702-711, 2001 — See Table-2 in this reference).  
• 
  
• PEARL #4: For practical purposes — I find the easiest way to define the QRS as being "wide" in an adult is — IF the QRS complex in any lead is clearly more than half a large box in duration (ie, Since each large box on ECG grid paper = 0.20 second — more than half a large box = ≥0.11 second).

Returning to today's initial ECG — although the QRS does not "look" to be overly wide — it actually measures 3 little boxes in duration in a number of leads (ie, QRS duration = 3 little boxes = 0.04 X 3 = 0.12 second ==> therefore the QRS is wide in today's initial ECG). To facilitate our assessment — I've added enlarged inserts of the QRS in leads V2 and V6 in Figure-4.

• PEARL #5: More than simply determining if QRS duration is ≥0.11 second — the reason to focus our attention on whether or not the QRS is "wide", is that we are trying to exclude the possibility of a ventricular rhythm.
• Be aware that one or more leads in our assessment may look deceptively narrow if the initial or terminal part of the QRS lies on the baseline in the lead being looked at (which is why, "12 leads are Better than One" ).
• It is for this reason that: i) I always look extra carefully when measuring QRS duration if a number of QRS complexes seem like they may be wider-than-they-should-be; — ii) We need to look carefully at all 12 leads at the onset and offset of the QRS when measuring (I find this easiest to do by selecting QRS complexes that either begin or end on an ECG grid line); — and, iii) We should choose as our QRS duration measurement the longest complex for which we can accurately determine the onset and offset of that QRS.  

Figure-4: I've added enlarged inserts of leads V2 and V6 from today's initial ECG that was shown in Figure-1. The vertical RED lines in leads V2 and V6 of these inserts mark the onset and offset of the QRS in these leads (which measures  3 little boxes = 0.12 second — therefore confirming a wide QRS).
= = = = =
NOTE: Doesn't the QRS look deceptively narrow in lead V3? This did not deter me from determining the true QRS duration — because I felt that each of the remaining 11 leads "looked" like they were wide. Seeing regular upright P waves with a fixed PR interval in lead II — then confirmed that the reason for QRS widening in today's case was some type of conduction defect (and not a ventricular rhythm).

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CASE Follow-Up:

• Today's patient has MBBB. This woman was extremely symptomatic at the time she presented to the ED with recurrent syncopal episodes. Eventually (ie, on her 3rd ED visit) — she experienced an extended episode of profound bradycardia consistent with PAVB (Paroxysmal Atrio-Ventricular Block) — as discussed in the ADDENDUM below.
• The patient was referred for permanent pacing.

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Acknowledgment: My appreciation to Ahmed Marai (from Irak) and Amr Elhelaly (from the UK) — for allowing me to use this case and these tracings.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation. 
• 
  
• ECG Blog #282 — reviews a user-friendly approach to the ECG diagnosis of the Bundle Branch Blocks (RBBB, LBBB and IVCD).
• 
  
• ECG Blog #203 — reviews ECG diagnosis of Axis, Hemiblocks and Bifascicular Blocks.
• 
  
• ECG Blog #394 and ECG Blog #419 — for 2 more examples of MBBB.

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ADDENDUM (This Addendum is reproduced from ECG Blog #419): 

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Looking closely at Figure-2 — I suspect this abbreviated rhythm strip represents a type of PD-PAVB (Pause-Dependent Paroxysmal AtrioVentricular Block).

• The patient's history of a number of episodes that presumably were short-lived with spontaneous recovery — is consistent with PD-PAVB.

PEARL #6: As described by Bansal et al (J Arrhythmia 35:870-872, 2019) — Bosah et al (Cureus 14[7]: e27092, 2022) — and Uhm et al (Heart Rhythm Case Rep 4(5):197-199, 2018) — the entity known as PAVB is a potential cause of syncope that is easily overlooked, and which is potentially lethal (probably more often than is commonly realized).

• PAVB is characterized by the sudden, unexpected onset of complete AV block with delayed ventricular escape — therefore resulting in a prolonged period without any QRS on ECG. Prior to the prolonged pause — the patient manifests 1:1 AV conduction without other evidence of AV block (which is why onset of PAVB is typically so unsuspected! ).
• Because of its totally unexpected onset and propensity to result in sudden death — PAVB is difficult to document and significantly underdiagnosed.
• Three mechanisms for producing PAVB have been described: i) Vagally mediated (ie, Vagotonic Block — as described in ECG Blog #61, with the references listed at the end that Blog post citing instances of transient asystole from excessive vagal tone!); — ii) Intrinsic (Phase 4 = pause- or bradycardic-dependent) PAVB; — and, iii) Idiopathic.

i) Vagotonic AV Block:

This form of PAVB is potentially benign when it results from a transient profound surge of parasympathetic tone in an otherwise healthy individual (as might occur with an episode of severe vomiting; a fit of severe coughing; vasovagal reaction from a blood draw).

• The problem with vagotonic PAVB is localized to within the AV Node.
• There will often be a "prodome" of diaphoresis, nausea, dizziness — with the patient aware of imminent fainting.
• 
  
• Characteristic ECG findings of vagotonic PAVB include progressive sinus rate slowing — often associated with an increasing PR interval and a narrow-QRS escape focus — followed by recovery with progressive return to a normal sinus rate and normal PR interval.

ii) Intrinsic PAVB:

Several names have been attached to this mechanism of PAVB — including most commonly "Phase 4 AV block" and/or PD-PAVB (Pause-Dependent Paroxysmal AtrioVentricular Block).

• PD-PAVB is the most likely mechanism for the cardiac rhythm in Figure-2 from today's case. The underlying pathology is severe His-Purkinje System disease (strongly suggested by the presence of MBBB in Figure-3 of today's case). This form of PD-PAVB is likely to be fatal unless the patient receives a permanent pacemaker.
• The interesting pathophysiology of PD-PAVB results from chance occurrence of an "appropriately-timed" PAC or PVC that partially depolarizes the diseased HPS (His-Purkinje System) at a specific point in the cycle that renders the poorly-functioning HPS unable to complete depolarization. The resultant prolonged pause in ventricular depolarization may only resolve if another "appropriately-timed" PAC or PVC occurs at the precise point needed to "reset" the HPS depolarization cycle (which presumably explains why the patient in today's case spontaneously recovered).
• Of note — although severe underlying HPS disease is evident from the bradyarrhythmia seen in Figure-2 of today's case — up to 1/3 of patients with PD-PAVB do not show evidence of conduction defects on ECG, thereby complicating documentation of this diagnosis.

iii) Idiopathic PAVB:  

This is the most recently described form of PAVB — in which findings are not consistent with either of the other 2 forms.

• The baseline ECG before idiopathic PAVB tends to be normal.
• No "trigger" for PAVB is evident (ie, no source of excessive vagal tone — and no precipitating PACs/PVCs are seen).

 

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.
• 
  
• 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).
• 
  
• 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).
• 
  
• 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.
• 
  
• 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).