ECG Blog #312 — Bigeminy but Not Mobitz I

How would YOU interpret the lead II rhythm strip shown in Figure-1?

Figure-1: How would you interpret this rhythm strip?

MY Approach to the Rhythm in Figure-1:

As always — I favor a systematic approach to every arrhythmia that I encounter, encompassed by the memory aid, "Watch Your Ps, Qs and the 3Rs" (See ECG Blog #185). That said, looking at this rhythm — I could not fail to notice that there is "group beating" in a supraventricular (ie, narrow QRS) bigeminal pattern.

PEARL #1: As discussed in ECG Blog #232 — recognition of a bigeminal supraventricular pattern when the 1st beat in each pair is conducted, should suggest the following differential diagnosis:

• Sinus rhythm with atrial or junctional bigeminy (ie, every-other-beat is a PAC or a PJC).
• Sinus rhythm with atrial trigeminy — in which every-third P wave is a PAC that is "blocked" (non-conducted).
• Some form of SA ( = Sino-Atrial) Block.
• Mobitz I, 2nd-Degree AV Block ( = AV Wenckebach) with 3:2 AV conduction.
• Mobitz II, 2nd-Degree AV Block (with non-conduction of every 3rd P wave).

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Beyond-the-Core: Technically, there are a few additional causes of a bigeminal rhythm that need not be considered in today's case, because the rhythm is either not strictly supraventricular — or — because the 1st beat in each group is not sinus-conducted. These additional causes include:

• Ventricular bigeminy (ie, every-other-beat is a PVC).
• Atrial fibrillation, atrial tachycardia or atrial flutter with Wenckebach conduction.
• "Escape-Capture" (the 1st beat in each group is a junctional or ventricular escape beat — followed by a conducted beat).

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PEARL #2: Another way to look at the bigeminal pattern of group beating that we see in Figure-1 — is that each group of 2 beats is separated by a short pause.

• The commonest cause of a pause is a blocked PAC. In clinical practice — the finding of blocked PACs is far more common than any form of AV block.
• As a result, within seconds of seeing today's tracing — my thoughts were that statistically, the most likely cause of the bigeminal rhythm with short pauses that is seen in Figure-1 — would be atrial trigeminy, in which every-third P wave is a blocked PAC. I'd therefore want to address this possibility early in my assessment. 

 

At this point — I applied the Ps, Qs, 3R Approach:

• P waves — are present (RED arrows in Figure-2 highlight upright sinus P waves in lead II).
• The QRS is narrow — which confirms that the rhythm is supraventricular.
• The rhythm in Figure-2 is not "Regular" — so the Rate varies. That said — there is group beating, with a repetitive pattern of alternating short-long intervals. P waves are Related to neighboring QRS complexes — in that each QRS complex in this tracing is preceded by a sinus P wave with a fixed and normal PR interval. However, the P-P interval is not regular.

Figure-2: I've added RED arrows to Figure-1 to highlight sinus P waves.

Continuing with My Systematic Approach to the Rhythm:

Now that we have systematically assessed the 5 parameters in the Ps, Qs, 3R Approach — it's time to consider the entities included in the differential diagnosis for a bigeminal rhythm that was presented above in PEARL #1:

• Despite the clinical reality expressed in PEARL #2 above — there is no evidence that the rhythm in Figure-2 represents atrial trigeminy, with every third beat being a PAC that is non-conducted. That is — there is no deflection suggestive of a non-conducted PAC in the T wave of beats #1, 3, 5, 7 and 9.
• The rhythm in Figure-2 is neither Mobitz I nor Mobitz II 2nd-degree AV block. The reason we can easily exclude 2nd-degree AV block — is that the atrial rhythm is not regular! (RED arrows in Figure-2). With rare exceptions, for there to be AV block — the P-P interval should at least be fairly regular, and this is definitely not the case in this tracing That is — no P wave is seen near the mid-point of each pause, as would be expected if some form of 2nd-degree AV block was present.
• Additional reasons why the rhythm in Figure-2 is not a form of AV block are: i) The PR interval is not increasing (as it should be if this was Mobitz I); and, ii) The QRS is not wide (as it should be if this was Mobitz II).
• 
  
• The rhythm in Figure-2 is not junctional bigeminy — because the P wave in lead II is positive everywhere (The P wave in lead II would be negative if there were junctional beats). This also rules out "escape-capture" — because there are no junctional escape beats.
• The rhythm is not atrial bigeminy — because P wave morphology of every P wave is the same (ie, with a distinct notch at its midpoint). In addition — the PR interval in front of every beat remains the same.
• 
  
• By the process of elimination — this leaves us to consider some form of SA block as a likely etiology for the rhythm in Figure-2.

CAVEATS (Beyond-the-Core): 

Unfortunately — We only have access to the 7 second rhythm strip that is shown in Figure-2. We do not have access to a simultaneously-recorded 12 lead ECG.

• It is true that PACs which originate near the SA node may closely resemble sinus P waves in one or more leads. Technically speaking, without the benefit of a 12-lead ECG — I can not completely rule out the possibility of atrial bigeminy, in which the reason the P waves before beats #1,3,5,7 and 9 so closely resemble the P wave of sinus beats — is that the PACs originate so near to the SA node.
• For the same reason — I can not completely exclude the possibility that the reason for the short pauses in Figure-2 might be blocked PACs that are not evident in the single lead being monitored. And although no notched deflection suggestive of a blocked PAC is seen in Figure-2 — it is true that the ST-T wave of beats #1,3,5,7 and 9 appears to be flatter than the ST-T wave of beats #2,4,6,8.
• 
  
• That said — I think the rhythm in Figure-2 is most consistent with SA Block.

The Concept of SA Block:

Wenckebach phenomena, in which there is progressive delay in conduction until conduction fails — is not limited to the Mobitz I type of 2nd-degree AV block that occurs out of the AV node.

• Among the other types of Wenckebach conduction — is SA Block of the Wenckebach type. Instead of progressive delay in the PR interval until eventually a P wave fails to conduct to the ventricles (as occurs with the Mobitz I form of 2nd-degree AV block) — with SA Wenckebach, there is progressive delay in the time it takes sinus node impulses to get out of the SA node — until eventually, exit of an impulse out of the SA Node is completely blocked.
• Because this progressive delay in sinus node impulses is completely contained within the SA node — SA block is not seen on the surface ECG. This makes it much more challenging to diagnose SA block.

The mechanism of SA Wenckebach is best explained by use of a Laddergram. I illustrate this concept in Figure-3 — in which I propose a laddergram to explain the ECG findings for today's rhythm:

• Note the addition in Figure-3 of an "extra" Tier to the laddergram — to illustrate progressive delay of sinus node impulses trying to get out of the SA Nodal Tier. Note that every-third SA nodal impulse is blocked.
• Of the 2 sinus node impulses in each group that are able to make it out of the SA Node — conduction of these impulses on their way to the ventricles now proceeds normally, as these impulses pass through the Atria — the AV Node — and the Ventricles. Thus, my proposed laddergram suggests that the rhythm in today's case represents SA Wenckebach with 3:2 SA conduction (ie, 2 out of every 3 SA nodal impulses is able to make it out of the SA Node).

Figure-3: My proposed laddergram for the rhythm in today's case.

NOTE: It may be easiest to think of SA block as an "exit" block that occurs at the level of the SA Node. In the same way that 2nd-degree AV block may be of the Mobitz I and Mobitz II types — so it is with SA block:

• With the Mobitz II form of AV block — instead of progressive increase in the PR interval until a beat is dropped, the PR interval remains constant until one or more on-time P waves is non-conducted.
• 
  
• With SA block of the Mobitz II type — sinus node impulses are conducted out of the SA Node without progressive delay — until suddenly, one or more on-time sinus node impulses is not able to make it out of the SA Node. As a result, with SA block of the Mobitz II type — the pause due to non-conduction of one or more P waves out of the SA Node will be some "fixed ratio" of the shortest P-P interval (ie, the result of 2:1, 3:1 or other ratio "exit" block). This is in contrast to SA Wenckebach — in which the pause is less than twice the shortest P-P interval

The "essentials" of SA Block are summarized in Figure-4. I emphasize the following:

• SA block is not common! I count on my fingers and toes the number of times I've seen true SA block over my decades of looking for this rhythm disorder. But as per my proposed laddergram in Figure-3 — I believe this is the most logical explanation for the mechanism of today's rhythm.
• The significance of SA block depends on the clinical setting in which it occurs. This may be a benign conduction disturbance when the pause containing non-conducted sinus impulses is short and occurs in an otherwise healthy and asymptomatic individual. In contrast — when associated with other conduction system disorders in a symptomatic patient with underlying heart disease — clinical outcome may be significantly influenced by the presence of SA block. In older individuals with syncope — SA block may be a component of Sick Sinus Syndrome. That said, given the absence of information in today's case — clinical significance (if any) of the rhythm in Figure-3 is unknown.

Figure-4: Essentials of SA Block (Modified from Grauer: ACLS-2013-ePub).

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #185 — Reviews the Ps, Qs and 3R Approach to Systematic Rhythm Interpretation.
• ECG Blog #188 — for Review on how to Read (and/or Draw) Laddergrams (with links to more than 50 examples of explained laddergrams).
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• ECG Blog #232 — Reviews the concept of a Bigeminal Rhythm (which may be due to Atrial or Ventricular Bigeminy, Wenckebach conduction — or other causes — Listen to Audio Pearl #47).
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• ECG Blog #163 — Reviews a case of "escape-capture" bigeminy, in which SA block might be operative.
• ECG Blog #256 — Reviews another case of "escape-capture" bigeminy (in which retrograde conduction from junctional escape results in "capture").
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• ECG Blog #164 — Reviews a case Mobitz I 2nd-Degree AV Block, with detailed discussion of the "Footprints" of Wenckebach.
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• ECG Blog #33 — Reviews a case showing blocked and aberrantly-conducted PACs. 
• ECG Blog #66 — Reviews a case showing blocked and aberrantly-conducted PACs. 
• ECG Blog #147 — Reviews a case showing blocked PACs. 
• ECG Blog #57 — Reviews a case showing atrial bigeminy with blocked PACs.

ECG Blog #311: The Culprit of the Rhythm?

The ECG in Figure-1 — was obtained from a middle-aged man who presented with shortness of breath. No chest pain. Assuming the patient was hemodynamically stable:

• How would YOU interpret the rhythm in Figure-1?
• What are your diagnostic considerations?

NOTE: This is a challenging case! Both the rhythm and the 12-lead ECG manifest complexities without simple solution. My hope is to provide insight by presenting my thought process in the sequence that I used to approach this tracing. Are YOU up for the challenge?

Figure-1: 12-lead ECG and long lead II rhythm strip recorded from a middle-aged man with shortness of breath. No chest pain.

My Thoughts on Figure-1:

Instinctively applying the Ps, Qs, 3R Approach for assessment of the rhythm in Figure-1 (See ECG Blog #185) — my initial impression of this tracing (that I made within the first minute or so of seeing this ECG) — was the following:

• The rhythm is supraventricular (ie, the QRS complex appears to be narrow in all 12 leads).
• The rhythm is not completely regular. That said — there does appear to be "group" beating (with longer and shorter R-R intervals of a duration that repeats). 
• P waves are present. I suspected that the atrial rhythm might be regular.
• At least some P waves appear to be conducting (because some PR intervals repeat a number of times in this tracing!).
• 
  
• My Initial IMPRESSION: The findings of group beating — with P waves that look like they might be regular — a narrow QRS — and, a number of PR intervals of similar duration — when taken together, suggest that some type of Wenckebach conduction (if not 2nd-degree AV block of the Mobitz I type) is likely.

What About the 12-Lead ECG?

At this point I found myself continually looking at the exceedingly tall T waves in the anterior leads of Figure-1. From a Clinical Perspective — highest priority in assessing any case, is to quickly determine IF immediate treatment is needed. In today's case — Clarification of the rhythm beyond my above brief analysis is probably not needed for initial treatment decisions. As long as the patient remains stable (and the overall heart rate does not drop) — it is unlikely that a pacemaker will be needed. As a result — our priority shifts to assessing the 12-lead ECG regarding whether prompt cath and/or thrombolytic therapy is needed.

• PEARL #1: An additional reason for turning our attention at this point to assessment of the 12-lead ECG — is that doing so may help in assessment of the rhythm (as I'll show momentarily).

Assessing the 12-Lead:

• There is low voltage in the limb leads (ie, QRS amplitude does not exceed 5 mm in any of the limb leads).
• The frontal plane axis is normal (Probably close to 0 degrees — though difficult to assess due to low voltage and Q waves of variable depth in the inferior leads).
• There is no chamber enlargement.
• There clearly has been a recent inferior MI (ie, Q waves are present in each of the inferior leads — in association with ST segment coving, at least 1 mm of ST elevation — and deep T wave inversion).
• R wave progression is normal in the chest leads — with transition (where the R wave becomes taller than the S wave is deep) — occurring normally between leads V2-to-V3.
• T waves are exceedingly tall and peaked in anterior leads V2, V3 and V4 (with a T wave = 15 mm tall in lead V3). 
• T waves are also disproportionately tall in leads I and aVL. 
• The ST-T wave is flat in lead V6.

My Impression of the 12-Lead:

Despite the absence of chest pain — this patient has had a recent inferior MI. Without more history — it is difficult to determine when this occurred. Q waves are already quite deep (especially in leads III and aVF). ST elevation persists — although the amount of ST elevation is almost overshadowed by the very deep, symmetric T wave inversion in each of the inferior leads. A mirror-image opposite picture to this inferior lead T wave inversion is seen in the shape of the disproportionately tall T wave in lead aVL.

• The composite picture in ECG #1 is consistent with a completed inferior STEMI from acute RCA (Right Coronary Artery) or possibly LCx (Left Circumflex) occlusion — now with reperfusion T waves in the inferior leads
• Admittedly, the tall, peaked anterior T waves resemble deWinter T waves in their size and shape. However, to postulate that these are deWinter T waves would imply acute involvement of a 2nd coronary artery (ie, the LAD = Left Anterior Descending coronary artery). I think it far more likely that these tall anterior T waves represent part of the same acute process (ie, acute occlusion of the RCA or LCx — and not of the LAD).
• 
  
• Acute inferior MIs are frequently accompanied by posterior involvement — in which the anterior leads show a mirror-image of events occurring in the posterior wall of the left ventricle. As a result — anterior leads show ST depression (instead of ST elevation) with acute posterior MI — and anterior leads show tall, peaked T waves (instead of deep T wave inversion) when the posterior wall is reperfused.
• 
  
• Putting It All Together: I suspect today's patient had a recent infero-postero STEMI — and is now showing reperfusion T waves in these lead areas (ie, in the form of deep T wave inversion in inferior leads — and tall, peaked T waves in anterior leads). 
• Additional history — serial troponins — Echo — and follow-up ECGs could all contribute to better understanding regarding the timing of this patient's event. Cardiac cath may be indicated — but given the ECG appearance in Figure-1 (that suggests this MI did not just happen) — cardiac cath will probably not be needed on an emergency basis as long as the patient remains stable.

PEARL #2: It is common to see 2nd-degree AV block of the Mobitz I type in association with acute or recent inferior MI. As a result — I immediately suspect some form of this conduction disorder in the setting of recent or acute inferior MI whenever I see group beating with a regular atrial rhythm and a number of similar PR intervals at the beginning of a number of groups. This is the situation in today's rhythm (See below).

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A Closer Look at Today's Rhythm:

I found assessment of today's rhythm extremely challenging. My point in the above discussion — is that regardless of whether you were able to determine the precise etiology for each beat in the long lead II rhythm strip of Figure-1 — my basic assessment described above (ie, that this supraventricular rhythm with group beating in association with recent inferior MI is likely to represent some form of 2nd-degree Mobitz I AV block) — is more than adequate for initial management of this patient.

That said — Let's look closer.

QUESTION: 

• Are the P waves in Figure-1 regular?

ANSWER — See Figure-2 ...

Figure-2: I've labeled the P waves in Figure-1 with RED arrows.

PEARL #3: As I have often emphasized — I have found the simple act of identifying all P waves to be invaluable for guiding me toward the right diagnosis.

• Using calipers greatly facilitates the process. Set your calipers to the P-P interval between any 2 P waves that you clearly see in the long lead II rhythm strip (For example — Set your calipers to the P-P interval between the 2nd and 3rd RED arrows in Figure-2 — or between the 3rd and 4th RED arrows). Doing so readily allows you to "walk out" this interval throughout the entire rhythm strip (RED arrows in Figure-2).

My Next Steps in Rhythm Analysis:

Now that we have verified that the atrial rhythm is regular (at a rate just over 100/minute) — LOOK again in Figure-2 at the QRS complexes that occur at the end of each of the longer R-R intervals (ie, at beats #3, 4, 6, 7, 9 and 10).

• Are each of these beats preceded by a P wave? IF so — Is the PR interval of the P waves in front of beats #3,4; 6,7; and 9,10 long enough to conduct?
• Is the PR interval identical before any of these beats?
• Finally — LOOK to see IF a P wave precedes beats #2, 5, 8 and 11? IF so — Is the PR interval before each of these beats the same or different?
• 
  
• PEARL #4: You are looking for relationships that suggest the arrangement in this long lead II rhythm strip is not by chance! Finding such relationships is very characteristic of the likelihood that some form of Wenckebach block is present!

Figure-3: I've labeled P waves in the long lead rhythm strip according to their relationship with neighboring QRS complexes (See text).

ANSWERS:

I noted the following relationships between P waves in the long lead II rhythm strip — and their neighboring QRS complexes (Figure-3):

• The P waves highlighted by WHITE arrows in Figure-3 all occur simultaneously with the onset of the QRS complex of beats #1, 4, 7 and 10. The PR interval of each of these WHITE-arrow P waves is clearly too short to conduct.
• 
  
• The P waves highlighted by RED arrows all manifest the same PR interval. These are the P waves before beats #3, 6 and 9. I measure the PR interval before these beats = 0.14 second, This is a long enough PR interval to conduct to the ventricles — although it is shorter-than-what-is-usually-seen for a patient with 2nd-degree AV Wenckebach. Because the PR interval in front of each of these beats is equal — I assumed that these RED-arrow P waves were conducting (but I could not be certain of this because of the relatively short PR interval).
• 
  
• The P waves highlighted by PINK arrows also all manifest the same PR interval, albeit a longer PR interval than that manifest by the RED-arrow P waves. These are the P waves before beats #2, 5, 8 and 11. I measure the PR interval before these beats = 0.24 second. I thought each of these PINK-arrow P waves were definitely conducting to the ventricles.
• 
  
• This left the 6 P waves highlighted by BLUE arrows — all of which occurred near the mid-point of one of the longer R-R intervals. I was not at all certain whether these BLUE-arrow P waves were conducting with a much longer PR interval — or whether they were not conducted.

NOTE: Today's rhythm is not typical for a simple Mobitz I, 2nd-degree AV block because: i) The PR interval before the QRS complex at the end of longer R-R intervals is not consistent as it usually is with typical Mobitz I (ie, alternating WHITE and RED arrows in front of beats #1, 3, 4, 6, 7, 9, 10); ii) The PR interval for RED-arrow P waves is shorter than is usually seen for conducting beats with Mobitz I ( = 0.14 second); and, iii) We never see 2 P waves in a row that are definitely conducting and manifesting progressive increase in their PR interval.

• Unfortunately — the long lead II rhythm strip in today's tracing is not simultaneously-recorded with the 12-lead ECG above it. This negates use of a very helpful potential clue — which is that junctional escape beats can sometimes be distinguished from conducting beats because they may manifest slightly different QRS morphology.

LADDERGRAM Illustrations (Beyond-the-Core):

In my attempt to explain the mechanism of today's arrhythmia — I propose 2 potential solutions below: 

I show the simplest explanation for today's rhythm in Figure-4a: 

• Most of the time with AV Wenckebach (ie, Mobitz I 2nd-degree AV Block) — there is a gradual increase in the PR interval with successive beats until a P wave is non-conducted. However, on occasion — dual AV nodal pathway physiology may be operative (Mani BC & Pavri BB: Dual AV Nodal Pathways Physiology — Indian Pacing Electrophysiol 14[1]:12-25, 2014). When this happens — there may be an abrupt change (increase) in the PR interval from one beat to the next due to sudden change in conduction from the fast pathway (which results in a shorter PR interval) — to conduction over the slower pathway (which results in abrupt PR interval lengthening). IF this is the mechanism in today's arrhythmia — it would look like the laddergram in Figure-4a.

Figure-4a: Proposed laddergram which presumes dual AV nodal pathway physiology — with abrupt switch to much slower conduction over one of the pathways accounting for the marked increment (increase) in PR interval from one P wave to the next — until a beat is dropped (ie, due to failed conduction over both AV nodal pathways).

I propose a 2nd potential explanation for today's rhythm in Figure-4b:

• It could be that the reason the WHITE-arrow P waves are not conducted — is that a junctional "escape" beat occurs before these P waves have a chance to conduct. Since the R-R interval preceding beats #4,7,10 is just over 5 large boxes in duration — this would correspond to a junctional "escape" rate at ~58/minute (which is within the usual 40-60/minute escape rate range of the AV Node).
• As shown in my proposed laddergram in Figure-4b — these junctional escape beats could be placed with a timing that also blocks conduction of the BLUE-arrow P waves occurring just before the WHITE-arrow P waves.
• These junctional escape beats might also account for why the PR interval of the PINK-arrow P waves is longer than the PR interval of RED-arrow P waves (as suggested by the dotted line retrograde conduction from these junctional beats within the AV Nodal Tier that prolong conduction through the AV Node of the PINK-arrow P waves).
• BUT — For the laddergram proposed in Figure-4b to be valid — the RED-arrow P waves would have to be able to conduct beats #3,6,9 with the relatively short PR interval = 0.14 second (which is a bit unusual in association with AV Wenckebach).

Figure-4b: My 2nd proposed laddergram for explaining the rhythm in today's case (See text).

PEARL #5: The path to achieving expertise in arrhythmia interpretation entails an appreciation of the following wonderful quote by Rosenbaum: “Every self-respecting arrhythmia has at least 3 possible interpretations.” 

• We need to accept that the surface ECG is not always able to explain the precise mechanism of every arrhythmia. As a result — there may be more than a single potentially valid explanation to a complex rhythm. This is not a "weakness" of the ECG — but rather acknowledgment of the clinical reality, that sometimes the only way to prove what the true mechanism for a complex arrhythmia is — is through additional ECG monitoring on the patient or by EP (ElectroPhysiologic) Study.
• 
  
• I could have postulated additional laddergrams for today's case. For example — since the R-R interval preceding beats #3,6,9 is about the same as the R-R interval preceding beats #4,7 and 10 — it could be that all 6 of these beats represent junctional escape. IF that were the case — it would eliminate having to postuate that the RED-arrow P waves are conducting with the relatively short PR interval = 0.14 second. But it would mean postulating that there are 2 junctional beats in a row.

BOTTOM LINE for Today's Case:

Clinically — As intellectually interesting as it is to postulate the mechanism for today's rhythm — the answer to this question is not essential for appropriate management of today's case:

• The initial ECG in Figure-1 tells us that this middle-aged man who presented with shortness of breath — most likely had a recent infero-postero MI that has evolved, and is now showing reperfusion T waves in the areas of infarction.
• As a consequence of this recent event — he manifests a complex form of 2nd-degree AV block with Wenckebach conduction — but fortunately, with an overall ventricular rate between ~60-70/minute. 
• There is no indication for pacing for the rhythm at this time. There is nothing to suggest that the conduction block is Mobitz II (especially since we never see 2 consecutively conducted P waves with the same PR interval). The rhythm is definitely not complete AV block because the ventricular rhythm is not regular — and there are several sets of repetitive PR intervals (which by definition would not be present if there was complete AV dissociation from 3rd-degree AV block).
• Additional treatment decisions (including whether to cath the patient — and if so, when to do so) — will not depend on determining a more precise diagnosis of the rhythm.
• 
  
• My HOPE — is that working through the above "thought process" will prove insightful for the process of interpreting a complex arrhythmia. I also think it worthwhile to appreciate when explanation of every beat on a tracing is not essential for appropriate initial management.

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Acknowledgment: My appreciation to Abdullah Al Mamun (from Dhaka, Bangladesh) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation (outlined in Figures-2 and -3, and the subject of Audio Pearl MP-23 in Blog #205).
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• ECG Blog #266 — Reviews a case illustrating distinction between deWinter T waves vs Posterior Infarction.
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• ECG Blog #193 — illustrates use of the Mirror Test to facilitate recognition of acute Posterior MI. This blog post reviews the basics for predicting the "culprit" artery. NOTE: The Audio Pearl in this post reviews the concept of why the term "OMI" ( = Occlusion-based MI) should replace the more familiar term STEMI. 
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• ECG Blog #80 — Reviews determination of the "culprit" artery and — application of the Mirror Test for recognition of acute Posterior MI.
• ECG Blog #246 — Reviews use of the "Mirror Test" to facilitate recognition of acute Posterior MI.
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• ECG Blog #193 — Reviews the concept of "OMI" ( = Occlusion-based MI) — with an Audio Pearl that reviews the basics for predicting the "culprit" artery.
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• ECG Blog #294 — Reviews a case to illustrate keep concepts regarding predicting the "culprit" artery — and appreciating when reperfusion occurs.
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• ECG Blog #228 — Reviews the concept of "Silent" MI.
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• ECG Blog #184 — illustrates the "magical" mirror-image opposite relationship with acute ischemia between lead III and lead aVL (featured in Audio Pearl #2 in this blog post).
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• ECG Blog #262 — Reviews a case of recent acute Infero-Postero MI with group beating from Wenckebach conduction and Low Voltage (with a list of the causes of Low Voltage).
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• ECG Blog #183 — Reviews a case of deWinter T Waves (with the Audio Pearl in this post discussing some variants of the deWinter T wave pattern). 
• ECG Blog #53 — Reviews another case of deWinter T Waves.
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• ECG Blog #186 — The AV Blocks (and when to suspect Mobitz I).
• ECG Blog #224 — Reviews a case of Mobitz I with Inferior MI.
• ECG Blog #262 — Another case of Mobitz I with Inferior MI.
• ECG Blog #226 — A case of dual-level Mobitz I with Inferior MI.

ECG Blog #310: A Special Hat Sign?

An acutely ill man in his 40s was admitted to the hospital. Suffice it to say that the patient was intubated — and that there was multi-organ involvement including effects from severe alcoholism, mental confusion, tenuous fluid balance — and significant ventricular dysfunction on Echo. His initial ECG is shown in Figure-1.

• How would you interpret this initial tracing?

Figure-1: Initial ECG of an acutely ill man in his 40s with multi-organ involvement (See text).

MY Thoughts on the Initial ECG in Figure-1:

The rhythm in ECG #1 is sinus at a rate of 90-95/minute (ie, a small but definitely-present upright P wave is seen in lead II — and negative sinus P waves are consistently seen in leads V1 and V2).

• Regarding Intervals: The PR interval is normal — and the QRS complex is narrow — but the QTc is markedly prolonged (especially in the lateral chest leads — the QT takes up ~2/3 of the R-R interval!).
• The frontal plane axis in ECG #1 is normal (about +60 degrees).
• There is no chamber enlargement.
• Small (probably insignificant) q waves are seen in multiple leads (ie, leads I,II,III,aVF; V4,V5,V6). R wave progression is slightly delayed (Transition, where the R wave becomes taller than the S wave is deep — occurs between leads V4-to-V5).
• 
  
• ST-T wave appearance is remarkable, in that ST segments are coved (although not significantly elevated) in multiple leads — with diffuse, wide and extremely deep T wave inversion.
• Especially in leads V4,V5,V6 (but also in several limb leads) — I found it difficult to determine where the baseline was!

My IMPRESSION of ECG #1: Sinus rhythm — a narrow QRS, but markedly prolonged QTc interval — diffuse ST segment coving (but probably not significant ST elevation) accompanied by wide and deep, symmetric T wave inversion — with a highly unusual picture in which it is difficult to determine where the baseline is.

• Starting with what ECG #1 is "not" — I did not interpret this tracing as suggestive of acute infarction. 
• Instead — the marked QTc prolongation — with diffuse ST-T wave abnormalities (ST coving; deep, wide and symmetric T wave inversion) that are not attributable to any specific anatomic area is highly suggestive of Takotsubo Cardiomyopathy (See ECG Blog #46 — for full discussion of this entity). The acutely ill state of today's patient, together with the report of significant ventricular dysfunction on Echo could certainly be consistent with Takotsubo (Clearly — specifics of the Echo would be needed to determine if the findings were or were not diagnostic of Takotsubo).
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• BOTTOM LINE: In addition to suspicion about Takotsubo Cardiomyopathy — I thought ECG #1 was strongly suggestive of the Spiked Helmet Sign.

Did YOU Recognize the Spiked Helmet Sign?

The common theme of today's case involving this patient with severe multi-system disease, with consideration of Takotsubo Cardiomyopathy and the Spiked Helmet Sign — is increased catecholamines!

• First described by Littman in 2011 (Letter to Mayo Clin Proc: 86 (12): 1245, 2011) — the Spiked Helmet Sign ( = SHS) is an uncommon and unique electrocardiographic finding, that is seen in patients with acute critical illness (such as described in today's case). The sign is typically associated with a high mortality. In addition to extensive acute MI, Takotsubo Cardiomyopathy, and cardiac arrest — other conditions that have been associated with SHS include intracranial hemorrhage, sepsis, severe metabolic disorders. Many other critical care conditions will doubtlessly be added to this list — as recognition of this important ECG sign becomes more widespread.
• As shown for the insert in the lower right part of Figure-2 — the name of this “dome-and-spike” pattern is derived from the Pickelhaube, a spiked helmet worn in the 19th and 20th centuries by Prussian and German soldiers, as well as by policemen and firemen. (The literal translation of “Pickelhaube” in German = “pointe” or “pickaxe” for Pickel — and “bonnet” for Haube.).

Figure-2: Features of SHS (Spiked Helmet Sign) that are seen in multiple leads from the initial tracing shown in ECG Blog #299. The insert with the spiked helmet is from Laszlo Littmann’s 2011 Letter to Mayo Clinic Proceedings. I have previously used this insert Figure to illustrate another case of SHS, in My Comment from the June 28, 2020 post of Dr. Smith's ECG Blog.

ECG Findings of Spiked Helmet:

• As described by Crinion, Abdollah & Baranchuk (Circulation 141:2106 — June 23, 2020) — the QRS-ST segment with the Spiked Helmet Sign is characterized by 3 specific components: i) Some elevation of the isoelectric line that begins before the QRS complex (ie, making up the first half of the helmet); ii) Then sharp ascent of the R wave (ie, the “spike” in the helmet); and finally; iii) Coved ST elevation of varying degree, that may mimic an acute ST elevation MI (ie, the second half of the helmet).
• One, two, or all 3 of these components may be seen in one or more leads on the ECG. Although initial reports limited the occurrence of this finding to the inferior leads — any of the 12 leads on an ECG may be affected!
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• PEARL #1: The proposed mechanism of the Spiked Helmet Sign (SHS) is fascinating — namely, a hyperadrenergic state with adrenergically mediated prolongation of repolarization. The reason for elevation of the isoelectric line beginning before the QRS complex — may result from similar pathophysiology as is seen in conditions with marked QT (and/or QU) prolongation — with the late and enlarged T and U waves being superimposed on the initial portion of the QRS. Other features shared with excessive endogenous catecholamine states (such as long QT syndrome, Takotsubo Cardiomyopathy and CNS hemorrhage) — include Torsades de Pointes, T wave alternans, and pseudo-infarct ST elevation.
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• PEARL #2: As noted above, the Spiked Helmet Sign (SHS) may produce ST elevation that might easily be mistaken for an acute STEMI. However, distinction from a STEMI can often be made by recognizing the upward shift of the isoelectric line that begins before the QRS complex — and which often comes close to “lining up” with the ST elevation seen after the QRS. This distinguishing feature is best illustrated within the PURPLE rectangle in the Spiked Helmet insert in the lower right part of Figure-2. 
• Further support that the ST elevation pattern of SHS is not the result of acute infarction may be forthcoming from: i) Atypical distribution of the QRS-ST segment changes on the 12-lead ECG; and, ii) A lack of the typical evolutionary pattern of ECG changes seen with true STEMI.
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• The tracing seen in the upper portion of Figure-2 is from ECG Blog #299. I've outlined in RED the features of the Spiked Helmet Sign that are seen in several leads of this ECG. Although the pre-QRS elevation component of SHS is admittedly subtle — Isn't the picture of pointed spikes with associated marked ST elevation and coving seen in multiple leads striking?

The Spiked Helmet Sign in Today's CASE:

For clarity in Figure-3 — I've put the initial ECG in today's case together with a follow-up ECG done 3 days later on this patient. The patient's clinical condition was improved at the time ECG #2 was obtained, although he was still extremely ill.

• WHICH leads in the initial ECG ( = ECG #1) — best show the Spiked Helmet Sign?
• What difference do you see in Figure-3 between the initial ECG — and ECG #2, that was obtained 3 days later when the patient showed signs of clinical improvement?

Figure-3: Comparison between the initial ECG — and a follow-up ECG does 3 days later after some clinical improvement.

ANSWER:

• In the initial ECG — the Spiked Helmet Sign is BEST seen in the lateral chest leads (leads V4,V5,V6) — but it is also suggested in leads II and aVF. The "mirror-image" of this sign is seen in lead aVR.
• For clarity — I've outlined in RED the 3 Components of the Spiked Helmet in lead V5 of ECG #1: i) Elevation of the isoelectric line that begins before the QRS complex (1st PURPLE arrow — making up the first half of the helmet); ii) Sharp ascent of the R wave (ie, the "spike" in the helmet); and, iii) Coved ST elevation after the QRS (ie, 2nd PURPLE arrow — making up the second half of the helmet). Note that the onset of the ST elevation almost "lines up" with the top point of the pre-QRS elevation.
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• In the follow-up ECG (ie, ECG #2, done 3 days later) — the heart rate, frontal plane axis, and QRS morphology in virtually all leads is similar (with exception of the flat line in lead V3 due to a lost lead connection). The markedly long QTc, ST segment coving and diffuse wide, deep T wave inversion persist — but the isoelectric baseline is returning! As a result — a clear Spiked Helmet Sign is no longer present in ECG #2. 

FINAL Tracing in Today's CASE:

What I found most interesting about the ECGs in today's case — was how quickly the ECG manifestations in ECG #1 developed.

• The patient had been seen 10 days earlier for a less severe illness. An ECG was done at that time ( = ECG #3 in Figure-4). What do YOU think?

Figure-4: Comparison of the initial ECG in today's case — with a "baseline" tracing done 10 days earlier for a less severe illness.

MY Thoughts on Figure-4:

The lead V3 electrode in the "baseline" tracing done 10 days earlier — is probably malpositioned (ie, the abrupt R wave increase from lead V2-to-V3 — followed by an equally abrupt decrease in R wave amplitude from V3-to-V4 does not make physiologic sense). That said — comparison of the frontal plane axis and QRS morphology in other leads is similar between the 2 tracings. But everything else is different!

• The rhythm in ECG #3 — shows marked sinus bradycardia and arrhythmia, with a PAC toward the end of the tracing.
• Given how slow the rate is — the QTc is probably no more than minimally prolonged.
• ST-T waves are diffusely flat — with no T wave inversion.
• The isoelectric baseline is flat throughout the entire tracing.

Today's CASE: Putting It All Together:

Seeing the "baseline" tracing from 10 day's earlier is highly insightful.

• The "theme" for the ECG changes in today's case is "catecholamine surge"! With the space of 10 days — this patient's ECG evolved in dramatic fashion from presumed catecholamine excess due to severe acute illness (with multi-organ involvement and need for prolonged mechanical ventilation) — including alcohol withdrawal, mental confusion with suspected Wernicke encephalopathy — and probable Takotsubo (ie, "Stress") Cardiomyopathy.
• The 1st ECG manifestation of catecholamine excess — is the significant increase in heart rate compared to the bradycardia in the earlier tracing.
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• Take-Home PEARL: The ECG picture in the initial tracing (ECG #1 in Figure-4) — shows marked QTc prolongation and diffuse ST coving with wide, deep T wave inversion, but without specific anatomic distribution. This ECG picture should immediately suggest the possibility of Takotsubo Cardiomyopathy. Loss of the isoelectric baseline in multiple leads should facilitate recognition of the 3 components of the Spiked Helmet Sign (outlined in RED in lead V5 of Figure-3). The common "theme" for the increase in heart rate and these ECG findings is catecholamine surge — which is completely consistent with the clinical presentation of today's patient.

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Acknowledgment: My appreciation to Jean Max Figueiredo (from Nova Iguaçu, Brazil) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #185 — Reviews my System for Rhythm Interpretation, using the Ps, Qs & 3R Approach.
• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation (outlined in Figures-2 and -3, and the subject of Audio Pearl MP-23-LINK in Blog #205).
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• ECG Blog #299 — Reviews a case of Shark Fin ST Elevation with the Spiked Helmet Sign — as a result of a CNS Catastrophe (subarchnoid hemorrhage).
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• ECG Blog #46 — Reviews a case (and the KEY ECG findings) of Takotsubo Cardiomyopathy.
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• ECG Blog #59 — Reviews a case of Giant T Waves.

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