EXTRA COPY — ECG Blog #517: Recurrent Syncope — EXTRA COPY

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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 given the feeling this patient had on awakening "that she was going to die" — the astute clinician should have suspected that the patient may have had a bradyarrhythmic form of AV block and monitored the patient in the ED (and depending on the history — potentially admitting the patient for 24 hours to monitor her rhythm).
• And even if nothing showed on those 24 hours of telemetry — given the diagnosis of MBBB — the patient should have been warned to promptly report any "dizzy episodes". Especially given subsequent "several dizziness episodes" over the next few weeks — the patient would 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 listen (ie, Today's patient waking up, feeling she was "about to die" — and then having 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". But since I've become aware of this entity — in my experience, it is not rare. Instead, I find this similar to the frequency of Brugada ECG patterns — Takotsubo Cardiomyopathy — and blocked PACs — in that each of those entities seemed "rare" to me until I became aware of them. And now that I've become experienced recognizing these entities — they are no longer "rare" (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. It takes less time to depolarize a smaller heart. Therefore, QRS duration will normally be ≤0.10 second up to ~12 years of age (Rijnbeek et al — Eur Heart J 22:702-711, 2001— See Table-2).
• 
  
• 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. Since each large box on ECG grid paper = 0.20 second — more than half a large box is ≥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 ==> the QRS is wide in today's initial ECG (See Figure-3).

Figure-3: 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 mark the onset and offset of the QRS in these leads — which = 3 little boxes in duration = 0.12 second, therefore confirming a wide QRS.

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CASE Follow-Up:

• Today's patient has MBBB. This woman was extremely symptomatic with recurrent syncopal episodes, and an extended episode of profound bradycardia consistent with PAVB (Paroxysmal Atrio-Ventricular Block). 
• She was referred for permanent pacing.
• 
  
• See the ADDENDUM below for more on PAVB.

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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 (The Addendum below reproduced from ECG Blog #419): 

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In follow-up to the Comment I have just received from H.S.Cho — I would expand on my description of the cardiac rhythm in ECG #1 from today's case.

• Given the history in today's case (ie, Sudden onset of the rhythm seen in ECG #1 — that within a minute spontaneously resolved) — Rather than "near ventricular standstill" — this rhythm is best described as PD-PAVB (Pause-Dependent Paroxysmal AtrioVentricular Block).
• 
  
• For clarity — I have reproduced Figure-1 from today's case.

Figure-1: The 2 ECGs in today's case. 

Paroxysmal AtrioVentricular Block (PAVB):

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 this 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 ECG #1 from today's case. The underlying pathology is severe His-Purkinje System disease (strongly suggested by the presence of MBBB in ECG #2 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 MBBB seen in ECG #1 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.
• 
  
• PEARL #4: In addition to seeing MBBB in ECG #2 — the fact that the atrial rate remains the same in both ECG #1 and ECG #2 is yet one more reason why the rhythm in ECG #1 does not represent simple vagotonic PAVB.

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).

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NOTE: The conduction disturbance shown in ECG #1 from today's case differs from that shown in ECG Blog #342 — in which the initial rhythm was AFib (ie, no P waves present for the first 6 beats in this tracing) — followed by a prolonged flat line pause (nearly 5 seconds in duration) — until finally a QRS complex preceded by a P wave (that may or may not have been conducting) was seen.

• Whether the prolonged flat line pause in this Blog #342 example represents another variation of PD-PAVB due to severe underlying disease of the His-Purkinje System — or reflects severe SA Node disease (ie, Sick Sinus Syndrome) — or most likely represents some combination of the two, is uncertain from the single ECG I was provided with.
• That said — the BOTTOM Line remains the same, namely that assuming nothing "fixable" is found — permanent pacing will be needed.

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).
• 
  
• 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.
• 
  
• 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).
• 
  
• 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):

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