ECG Blog #449 — Isorhythmic AV Dissociation?

The ECG in Figure-1 — was obtained from a 45-year old man with diabetes, who was being treated for septic shock.

QUESTIONS:

• How would YOU interpret the ECG in Figure-1?
• What is the rhythm?
• Why does QRS morphology in the long lead II rhythm strip change every-other-beat?

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

MY Thoughts on the ECG in Figure-1:

This is a challenging ECG to interpret because of: i) the changing QRS morphology; and, ii) the difficulty in seeing all of the P waves. That said — I was able to determine the rhythm within seconds because of the following observations:

• All beats on this ECG are supraventricular! The "beauty" of having a 12-lead tracing with a simultaneously-recorded long lead II rhythm strip — is that this allows us to view each of the 12 beats on this tracing in 3 other simultaneously-recorded leads. Doing so confirms that even though there are 2 distinct QRS morphologies in the long lead II rhythm strip (especially obvious in lead III) — the QRS is narrow in all 12 leads. Therefore — the rhythm is supraventricular!
• There is group beating! (seen in Figure-1 in the form of a bigeminal rhythm, in which the same shorter — then the same longer R-R interval alternates throughout the tracing).
• Regular P waves are present throughout the entire tracing. This KEY observation can be verified within seconds — simply by using calipers (See Figure-2).

Figure-2: I've added RED arrows to the initial ECG — showing that regular P waves are present throughout the entire tracing.

PEARL #1: The clinician who does not use calipers to interpret complex arrhythmias like today's tracing — will invariably take more time for their interpretation, only to discover that they will never be certain about the regularity of atrial activity.

• To optimally assess atrial activity — I simply set my calipers to the P-P interval between any 2 consecutive P waves that I can clearly identify. For example, in Figure-2 — 2 consecutive P wave deflections are clearly seen to occur at the same place within each of the longer R-R intervals (so that I chose to set my calipers to the P-P interval between the 3rd and 4th RED arrows in Figure-2).
• Once I set my calipers to this P-P interval — I was able to easily "walk out" regular P waves throughout the entire long lead II rhythm strip.
• PEARL #2: The reason today's tracing is so challenging — is that every 3rd P wave is so well hidden within the T waves of every odd-numbered beat. This is where awareness of simultaneously-recorded leads may prove invaluable! Although we do not see every 3rd P wave in the long lead II rhythm strip (because these P waves are hidden within the T waves of beats #1,3,5,7,9 and 11) — we do see an "on-time" tiny negative deflection right after the 1st T wave in lead V1 (2nd RED arrow in lead V1). This confirms that P waves are hidden at a similar point in the T wave of all odd-numbered beats. Therefore — there is an underlying regular atrial rhythm, with sinus P waves at ~110/minute.

PEARL #3: Today's rhythm does not represent complete AV block (and it does not represent isorhythmic AV dissociation). We can quickly determine this by focusing our attention on the PR interval just before the QRS complex of each beat that ends each of the longer R-R intervals (ie, the PR interval before beats #3,5,7,9 and 11).

• Labeling P waves (as we have done with RED arrows in Figure-2) — greatly facilitates this process — and expedites us being able to tell that although the PR interval before beats #1,3,5,7,9 and 11 is slightly prolonged (ie, ~0.22 second) — this PR interval in front of all odd-numbered beats remains constant! Therefore — there clearly is at least some conduction.
• PEARL #4: Despite the finding of a regular atrial rhythm — there are more P waves than QRS complexes (ie, there are 18 RED arrow P waves in Figure-2 — but only 12 QRS complexes). This means that some form of 2nd-degree AV block must be present — since not all P waves are being conducted to the ventricles.

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PEARL #5: At this point in my interpretation — I was virtually certain that today's rhythm represented some form of AV Wenckebach (ie, 2nd-degree AV block of the Mobitz I Type) — because of the information the above-described 5 Observations told me:

• Observation-1: The QRS complex for all beats in all 12 leads of Figure-2 is narrow. Therefore — today's rhythm is supraventricular.
• Observation-2: There is group beating (in the form of alternating longer-then-shorter R-R intervals). The presence of "group beating" should always raise the possibility of Wenckebach conduction — IF certain other features are also present.
• Observation-3: The underlying atrial rhythm is regular (RED arrows in Figure-2). Knowing there is a regular sinus rhythm rules out the non-Wenckebach causes of group beating, such as atrial bigeminy.
• Observation-4: At least some beats are being conducted to the ventricles (because the PR interval is constant before all of the beats that end longer R-R intervals). As per PEARL #3 — since at least some P waves are being conducted to the ventricles — this rules out 3rd-degree (complete) AV block!
• Observation-5: There are more P waves than QRS complexes. This means that some of the regularly-occurring sinus P waves are not being conducted (which means some form of 2nd-degree AV block must be present).

MY Impression of ECG #1: The above 5 Observations confer ECG features that characterize "the Footprints of Wenckebach!" — which is why within seconds of seeing today's ECG, I was virtually certain there was some form of 2nd-degree AV Wenckebach (See ECG Blog #164 — ECG Blog #55 — ECG Blog #347 — and ECG Blog #154).

• That said — I had not yet demonstrated cycles with progressive increase in the PR interval until an on-time sinus P wave is dropped (as should be seen with typical AV Wenckebach).

For Practical Purposes: I would be happy IF you stopped at this point, knowing that the above 5 observations make it virtually certain that today's rhythm represents 2nd-degree AV block of the Mobitz I Type ( = AV Wenckebach).

• Beyond-the-Core: Take a LOOK at Figure-3 — in which I have used 3 colors to label a certain P wave pattern in this tracing that repeats itself over the 12 beats in the long lead II rhythm strip. What does each color signify?

Figure-3: I've used 3 colors to label all P waves in today's rhythm. What does each color signify?

The Colors in Figure-3:

It's easiest to break down what is happening in Figure-3 — by starting with the RED arrow P waves.

• As noted above in Observation-4 — the RED arrow P waves in Figure-3 all manifest the same 0.22 second PR interval. Therefore — beats #1,3,5,7,9 and 11 are all conducted with 1st-degree AV block.
• IF the rhythm in Figure-3 is AV Wenckebach — then either the PINK or the YELLOW arrow P waves must not be conducted. Doesn't it seem more logical for the YELLOW arrow P waves to be non-conducted? (which would mean that the PINK arrow P waves would be conducting beats #2,4,6,8,10 and 12 with a very long PR interval of ~0.38 second).

PEARL #6: The last 2 features to explain regarding today's ECG are: i) Why QRS morphology changes slightly with every-other-beat; and, ii) What the rest of today's 12-lead ECG shows.

• Since we know that all beats in today's tracing are supraventricular (Observation-1 in PEARL #5) — and since all QRS complexes are conducted — the reason for slight change in QRS morphology every-other-beat must be the result of some aberrant conduction. As explained in ECG Blog #211 — whether a beat does or does not conduct with some aberration depends on the interplay between coupling intervals and the preceding R-R interval. Although I do not see a specific form of conduction delay in the slightly wider QRS complexes (which are the odd-numbered beats) — the differing R-R intervals most probably accounts for the aberrant conduction.
• Mobitz I 2nd-degree AV block is commonly seen in association with acute or recent inferior and/or posterior infarction. That said — I thought ST-T wave appearance in the rest of the 12-lead ECG showed nonspecific (nondiagnostic) abnormalities. I did not see evidence on this tracing for recent or acute MI (but it is always important to look for ECG signs of recent inferior and/or posterior MI whenever you encounter Mobitz I 2nd-degree AV block).

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Laddergram Illustration:

The BEST way to prove that today's rhythm is 2nd-degree AV block of the Mobitz I (AV Wenckebach) Type — is to construct a laddergram, which I illustrate step-by-step in Figures-4 thru -10.

Figure-4: I find the easiest 1st step in drawing a laddergram is to complete the Atrial Tier, that shows atrial activity.

Figure-5: I next fill in the Ventricular Tier — which corresponds to the timing of those ventricular beats I am sure about. Since we know in today's tracing that all 12 beats are supraventricular — I drew the arrow for each of these QRS complexes in the Ventricular Tier facing downward (representing normal conduction of supraventricular impulses through the ventricles).

Figure-6: We are now ready to begin solving the laddergram. I do this by connecting those P waves from the Atrial Tier — to those QRS complexes that I am certain each of these P waves is conducting to (BLUE lines that I've drawn within the AV Nodal Tier).

Figure-7: It seems logical that the next P waves to conduct to the ventricles are those that are highlighted by BLUE arrows in this Figure-7. It should now be easy to see that conduction of this 2nd P wave in each group takes a bit longer to be conducted, which is the principal characteristic of Wenckebach conduction (BLUE lines that I've drawn within the AV Nodal Tier).

Figure-8: By the process of elimination — this means that the remaining BLUE arrow P wave is not conducted (ie, there are no unconnected QRS complexes left). This therefore "completes" the laddergram — by the "butt end" that I've added to the remaining BLUE arrow P waves.

Figure-9: For clarity — I now labeled each of the P waves in the long lead II rhythm strip with the same colors that I used above in Figure-3.

Figure-10: Most of the time when I draw a laddergram — I use the same color for all lines in the illustration, as shown here.

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Acknowledgment: My appreciation to Vansh Verma (from New Delhi, India) for the case and this tracing.

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Related ECG Blog Posts to Today’s Case:

• ECG Blog #185 — My Ps, Qs, 3R System for Rhythm.
• ECG Blog #188 — Reviews how to read and draw Laddergrams (with LINKS to more than 100 laddergram cases — many with step-by-step sequential illustration).

• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.

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• ECG Blog #192 — The 3 Causes of AV Dissociation. 
• ECG Blog #191 — AV Dissociation vs Complete AV Block.
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• ECG Blog #389 — ECG Blog #373 — for review of some cases that illustrate "AV block problem-solving".
• ECG Blog #236 — for an ECG Video Pearl on the 3 Types of 2nd-degree AV block.
• ECG Blog #344 — thoroughly reviews the Types of 2nd-degree AV block (Mobitz I vs Mobitz II vs 2:1 AV Block).
• 
  
• ECG Blog #267 — Reviews with step-by-step laddergrams, the derivation of a case of Mobitz I with more than a single possible explanation.
• ECG Blog #164 — Step-by-Step laddergram of Mobitz I.
• 
  
• ECG Blog #195 — reviews Isorhythmic AV Dissociation.

 

 

ADDENDUM (10/2/2024) — Based on Question by Akash

For those readers who enjoy the challenge of drawing laddergrams — I've decided to publish the Question sent to me from Akash (in the Comments below).

• As I've often emphasized — there may on occasion be more than a single possible explanation for the mechanism of a given complex arrhythmia!
• IF you are able to "draw" your theory for a potentially plausible mechanism — then consider yourself correct in proposing an alternative mechanism (in which case — the only way to verify which proposed mechanism is correct for the case at hand would be by EP study).
• The reason I thought it worthwhile to publish the excellent question that Akash asks — is that it illustrates the problem-solving process for complex rhythms, in which I have to "play" with a few potentially plausible laddergram solutions until I am able to come up with one that works.

This is the question by Akash (that I copied from the Comments below):

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Hello Dr. Grauer!
Long time lurker (and learner) here, posting for the first time.

• Could this be a 2:1 AV block?
• The first P wave (labelled with a RED arrow in Figure 3) is conducted (albeit with a slightly prolonged PR interval).
• The next P wave (the one hidden within the T wave = PINK arrow) is not conducted.
• The QRS complex labelled beat #2 is a junctional escape beat.
• The third P wave (YELLOW arrow) fails to conduct — because it finds the distal conduction system refractory (because of the junctional escape beat).

Is this a reasonable explanation of this rhythm? I’m sure I’m missing something, but am unsure what that is. Please throw light, Dr. Grauer!
Warm regards — Akash

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MY Reply to Akash:

Your question Akash is an excellent one — and I actually thought of the solution you propose when first working through this case.

• The problem however — is that if the 2nd P wave (first YELLOW arrow in Figure-11) was non-conducted because of 2:1 AV block and if beat #2 was a junctional escape beat — this would mean that you are proposing an accelerated junctional escape rate (because the R-R interval before beat #2 that you are proposing is junctional = 3.7 large boxes — which corresponds to an accelerated junctional escape rate of ~81/minute).
• And — this would mean that unless inhibited by a sinus-conducted beat — the next junctional escape beat would occur 3.7 large boxes later = where I placed the BLUE circle. But since the next sinus P wave is set to occur where the 3rd RED arrow occurs — we can see that this next junctional beat would prevent the 3rd sinus P wave from conducting .... (You'd have to propose "takeover" of the rhythm by an accelerated junctional rhythm — which I would not expect given the constant and reasonable PR interval before beats #1,3,5,7,9,11).
• 
  
• P.S.: Accelerated junctional rhythms and junctional tachycardia can occur — but they are relatively uncommon in adults unless there is some underlying cause (ie, ischemia, shock, electrolyte disorders, post-cardiac surgery, etc.).

BOTTOM Line: I thought it unlikely that there was 2:1 block with a "usurping" accelerated junctional rhythm. I also thought the laddergram that I derived in Figure-10 looked perfectly plausible for 2nd-degree AV Block, Mobitz Type I ( = AV Wenckebach).

Figure-11: Unsuccessful proposed laddergram (See above).

 

ECG Blog #448 — A Young Man with Chest Pain ...

The ECG in Figure-1 was obtained from a previously healthy man in his early 20s — who initially presented with GI symptoms, that then evolved into CP (Chest Pain).

• The patient was thought to have anxiety.

QUESTIONS:

• Given the above history — How would YOU interpret the initial ECG that is shown in Figure-1?
• Does the patient's age infuence your interpretation?

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

ANSWERS:

As emphasized in ECG Blog #205 — I favor a 2-Step Process for the interpretation of any ECG:

• STEP #1 = Descriptive Analysis — in which we simply assess the 6 KEY Parameters of Rate — Rhythm — Intervals (PR-QRS-QTc) — Axis — Chamber Enlargement — and Q-R-S-T Changes — but without yet commenting on what this assessment might mean clinically.
• STEP #2 = Clinical Impression — in which we correlate our assessment that we made in Step #1 to the clinical situation at hand. For example, considering whatever symptoms that the patient may have had (ie, chest pain, palpitations, shortness of breath, etc.) — what this might mean in view of the ECG we are looking at.

KEY Points:

• Use of this systematic 2-Step approach does not slow you down. On the contrary — it speeds you up, because once you routinely incorporate a sequential, systematic approach — you'll find you no longer go back-and-forth looking at the ECG to see if you missed anything.
• 
  
• PEARL #1: My assessment of the 6 KEY Parameters is the same — regardless of the age of the patient. That said — What (if anything) these ECG findings that you identify might mean — will depend on your clinical correlation in Step #2.
• 
  
• PEARL #2: The reason it helps to know the age of the patient and the reason the ECG was done as soon as possible — is that it greatly facilitates Clinical Correlation. For example, in today's case — Knowing the patient is a younger adult who developed chest pain immediately increases our need to consider acute myocarditis in the differential diagnosis.

Figure-2: I've labeled the initial ECG. 

MY Interpretation of Today's Initial ECG:

I've labeled key findings in Figure-2 for today's initial ECG:

• The rhythm is sinus tachycardia at ~105/minute. 
• All intervals (PR, QRS, QTc) are normal. 
• The frontal plane axis is normal at about +70 degrees. 
• Given the patient's young adult age — QRS amplitude does not satisfy criteria for chamber enlargement.

Regarding Q-R-S-T Changes:

• Small and narrow Q waves are seen in the inferior leads, and in lead V6. These are likely to be normal septal q waves. (The initial deflection in lead aVL is positive — so there is an rSr' complex, but no Q wave in this lead).
• R wave progression — is normal, with progressive increase in R wave amplitude (albeit transition is slightly delayed until lead V5, when the R wave finally becomes taller than the S wave is deep).

There are subtle-but-important ST-T wave findings:

• My "eye" was drawn first to the 2 leads within the RED rectangle (ie, leads V5 and V6 each show 2 millimeters of J-point ST elevation — which is more than is usually seen with a normal repolarization pattern).
• There is a lesser amount of ST elevation in lead V4 — but given my concern about leads V5,V6 — I thought the ST-T wave in lead V4 showed some ST segment straightening, and was disproportionately larger-than-it-should-be with respect to the modest-sized R wave in this lead (within the BLUE rectangle).
• Normally, there is slight, gently upsloping ST elevation in leads V2 and V3. While I thought the ST-T wave in lead V3 was non-diagnostic — lead V2 lacks the slight amount of gently upsloping ST elevation that is usually seen in this lead.
• In the limb leads — there is slight-but-real J-point ST elevation in the inferior leads and in lead I (BLUE arrows) — with ST segment straightening in these same leads (as shown by the light BLUE lines).

STEP #2 = My Clinical Impression of ECG #1:

I had been sent this ECG with only the information that I noted in the above history (ie, that the patient was a previously healthy man in his early 20s — who presented with GI symptoms — that evolved into chest pain thought to be the result of anxiety).

• I wrote back, "This is not a normal ECG". I then specified the findings I cite above in my Descriptive Analysis.
• The sinus tachycardia is a definite concern that something acute may be ongoing. Almost all leads show some ST elevation — with more ST elevation in leads V5,V6 than is usually seen with early repolarization and, with abnormal straightening of the ST segment takeoff in multiple leads.
• 
  
• To Emphasize: I was not at all certain about what might be going on here. But what I wrote back was the following: "This could be acute LAD occlusion (ie, acute LAD OMI). Given that this patient is having CP — more evaluation is clearly needed. Alternatively — this could represent acute infero-postero-lateral OMI. In any event — I'd repeat the ECG within 10-20 minutes (and serially thereafter) — check Troponin — and would definitely follow-up until a definite answer is forthcoming! 
• Pericarditis is rare — but myocarditis is not, so especially in this age group — more information is needed to quickly determine if this could be an acute MI, myocarditis, or none of the above. Let me know what happened".

CASE Follow-Up:

The emergency physician recognized the abnormal ECG findings that I highlight above — and sent the patient to a PCI-capable center.

• Unfortunately — the cardiologist at that center did not recognize the abnormal ECG findings. The patient was discharged without repeating the ECG.
• The patient arrested outside the hospital. He could not be resuscitated.

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There are Lessons-to-be-Learned from today's case:

• Treat the patient — Not the age of the patient!
• Acute MI can occur in a younger patient.
• There are other potentially serious causes of CP in a younger adult. Some of these other causes may also be potentially life-threatening.
• IF at all concerned by the history and/or appearance of the patient — Do not allow your decision-making to be determined by a single ECG. I fully acknowledge that I was not certain from today's initial ECG that this patient had a life-threatening problem. That said — a series of subtle but potentially concerning findings are present in today's initial tracing — and, this should signal the need for additional evaluation until a clear diagnosis is forthcominng.
• Be systematic in your ECG interpretation. If the interventionist would have been systematic — the abnormal ECG findings highlighted in Figure-2 would have been identified.
• Sometimes cardiac cath is needed to distinguish between an MI vs myocarditis.

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PEARL #3:  Acute MI Can Occur in a Younger Patient!

To quote Dr. Stephen Smith: "The worst risk factor for a bad outcome in acute MI is young age." This is because clinicians (including too many cardiologists) have trouble accepting the fact that a young patient can have an acute MI (See case discussion in the January 9, 2023 post in Dr. Smith's ECG Blog — with links at the bottom of this post to a series of more cases illustrating this phenomenon).

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I have excerpted a portion of My Comment from this same January 9, 2023 post — regarding acute MI in a younger patient:

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“Treat the patient — Not the age of the patient”

The tendency to discount new chest pain in a young adult as the 1st symptom of acute MI is understandable. Acute coronary occlusion almost always occurs in patients who are beyond their 20s. That said — acute MI does occur in younger patients.

• There is a literature on this subject (Sood et al — Cureus 15(4):e37102, 2023 — Gulati et al — Mayo Clin Proceed 95(1):136-156, 2020 — GGF van der Schoot et al: Neth Heart J 28(6):301-308, 2020 — and — Egred at al — Postgrad Med 81(962): 741-745, 2005 — to name just a few reports). 
• Acute MI in younger patients may result from acute coronary occlusion — which can be precipitated by conventional risk factors (such as smoking begun at an early age) — in individuals with special predisposition (ie, a factor V Leiden mutation — or nephrotic syndrome — both being correlated with a hypercoagulable state) — and/or in familial entities such as genetic hypercholesterolemia.
• In addition — there is a series of nonatherosclerotic potential causes of acute infarction in younger patients. These include coronary artery spasm (as may be precipitated by cocaine use or binge alcohol drinking) — myocardial bridging (that may be the cause of intermittent acute ischemia) — aberrant anatomy of a coronary artery (which may present with sudden rupture causing acute infarction or sudden death at any age!).
• Other types of nonatherosclerotic potential causes of acute infarction in younger patients include systematic inflammatory disease (ie, lupus, rheumatoid arthritis, Wegener granulomatosis) — thrombosis not due to coronary disease (ie, endocarditis, coagulation disorders) — pregnancy (with its hypercoagulable state).
• Causation of Endothelial damage is another potential mechanism of acute MI in a younger patient. This may occur as a result of blunt chest trauma or other acute stress that produces a sudden extreme shear force on a coronary artery (that can result in an intimal tear that leads to intraluminal thrombosis). Endothelial damage may also be seen with spontaneous dissection of a coronary artery — or result from “deceleration trauma (ie, from an auto or other vehicular accident).
• 
  
• BOTTOM LINE: While the above etiologies are not common causes of acute infarction in an adolescent or young adult — they do occur! And, like most diagnostic considerations in medicine — if the differential diagnosis excludes such "other potential etiologies" simply because they are not common, or because the patient is "too young to have a heart attack" — then these other potential etiologies will be missed!
• 
  
• RELEVANCE to this Case: Although the young adult in today’s case presented with GI symptoms (that were thought to be exacerbated by anxiety) — this did evolve into frank CP. So, while today's history by itself is not particularly suggestive of an acute coronary event — in association with the abnormal ECG findings and persistent CP — additional evaluation was clearly indicated.
• 
  
• P.S.: Given the history in today's case, and the abnormal ECG findings — acute myocarditis needs to be included in diagnostic considerations. There are times when distinction between acute myocarditis vs acute OMI in a younger patient with acute-looking ECG changes and troponin elevation can only be made by cardiac catheterization. At other times, when strongly suspecting acute myocarditis and not acute MI — cardiac MRI may yield a definitive enough picture to confirm acute myocarditis as the diagnosis.

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Acknowledgment: My appreciation to Kashif Aleem (from Sargodha, Punjab, Pakistan) for the case and these tracings.

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Challenging Rhythms in 12yo — MIS-C Case Report

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Review of ECG Rhythms — MIS-C Case Report (9/16/2024):

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What follows below are my first impressions of the ECG rhythms sent to me from the Case Report by Dimah Jarmakani et al — of a 12-year old boy with MIS-C (Multisystem Inflammatory Syndrome in Children).

• For full discussion of the case — CLICK HERE — 
• User-friend link = tinyurl.com/KG-Blog-MIS-C —

CASE Overview (by Dr. Jarmakani):

A 12-year-old boy was admitted to our hospital with severe myocardial dysfunction and chaotic rhythm with tachy- and bradycardic arrhythmias. What follows are the ECG tracings of our patient:

• ECGs #1 and #2 were performed on the 2nd and 4th hospital days, respectively — at which time the patient had severe myocardial dysfunction. 
• ECGs #3,4,5,6 were done one week later — at which time the patient began to respond to the medical treatment, with recovery of myocardial function. 

We requested assistance from Dr. Grauer for interpretation of the ECG tracings, This is his response to us: 

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My impressions of representative tracings from this case:

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ECG #1:

Figure-1: ECG #1 is from the 2nd hospital day.

MY Thoughts on ECG #1:

This clearly is a challenging series of arrhythmias — obtained from this acutely ill 12-year old boy with MIS-C:

• I put limb leads and chest leads from this first tracing togeter (these tracings were sequentially recorded). Note that this tracing was recorded at half standardization. 
• The rhythm is highly variable. The RED arrow looks like a sinus P wave in front of beat #2. We really do not see more sinus P waves in this ECG #1 — but having glanced ahead at ECG #2, there clearly are sinus-appearing P waves in this next tracing (below) — so I’ll suppose that the RED arrow in front of beat #2 in ECG #1 is a sinus P wave (or possibly a P wave from another atrial focus).
• Given that this RED arrow P wave is pointed — I think we are seeing the opposite picture under each of the YELLOW arrows! I therefore suspect these YELLOW arrows highlight the location of retrograde conduction from ventricular beats.
• QRS morphology of beats #3,4; 6,7; 9,10; 12,13 and 15 shows marked right axis with an rS in lead I — and qR pattern in leads III,aVF.
• Unfortunately — we do not know for certain which beats in the limb leads correspond to which beats in the chest leads — but my guess is that beats #3,4; 6,7; 9,10; 12,13 and 15 with LPHB-like conduction — correspond to the RBBB-like beats in lead V1 of the chest leads. These beats are very wide and not preceded by P waves — so I think these are all PVCs (with a bunch of ventricular couplets) — and with the YELLOW-arrow retrograde conduction. RBBB-LPHB-like conduction suggest these may be fascicular beats from the left anterior hemifascicle (although the QRS is wider than fascicular beats usually are).
• In the chest leads of ECG #1 — we also see a LBBB-like etiology for beats #6 and 13 in the chest leads. It is hard to say if these are PVCs from another ventricular focus (though their close resemblance to LBBB conduction suggests to me that they may be supraventricular beats with aberration).
• I think the BLUE arrows in ECG #1 represent conducted beats from a different atrial focus (ie, these P waves being negative or not well seen in lead II — but better seen in other leads).

BOTTOM Line for ECG #1: 

• As interesting as the above details are — I do not think this matters clinically. The overall rhythm is chaotic — which is not necessarily unexpected given the history of an acutely ill 12-year with severe dilated cardiomyopathy on Echo. 
• I’d guess the overall rhythm is sinus, perhaps with a wandering atrial pacemaker and very frequent ventricular ectopy with multiple couplets. 
• The rhythm is not MAT — because pure MAT should show a different-shape P waves with every beat, which is not what we see here. That said — there is a spectrum of disorders with sinus rhythm and PACs at one end — and true MAT at the other end. This rhythm fits somewhere in between these 2 ends of this spectrum — and it is readily explained by the severe, acute illness of this child.
• As to interpretation of the 12-lead ECG itself — in both ECG #1 (and because of the scarcity of normally conducted beats in this initial tracing — I looked ahead at ECG #2 ) — the diffuse T wave inversion in inferior and all chest leads may be consistent with acute myocarditis as another component of the patient's MIS-C.

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ECG #2:

Figure-2: ECG #2 is from the 4th hospital day.

MY Thoughts on ECG #2:

Once again — the limb leads and chest leads are not simultaneously recorded. As noted in the Figure legends — ECG #2 was recorded on the patient's 4th hospital day (or 2 days after ECG #1 was recorded).

• NOTE: ECG #2 was recorded with double standardization!
• Even accounting for double standardization — sinus P waves in lead II (RED arrows) are tall and peaked, consistent with RAA (which is consistent with this patient’s underlying heart disease).
• After 2 sinus beats — we see junctional escape at a slow escape rate at ~40/minute. This is followed by 2 more sinus beats, and then another slow junctional escape beat.
• Given the young age of this patient — rather than SSS (Sick Sinus Syndrome) — I'd suspect some other underlying (and hopefully "fixable" ) cause of these rhythms, such as rate-slowing medication, electrolyte disturbance or hypoxemia.
• I suspect that best treatment for the rhythm disturbances seen thus far will be treatment of this patient’s underlying heart disease — which is easier said than done. In the meantime, a pacemaker may be needed if the rhythm slows further.

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ECG #3:

Figure-3: ECG #3 — obtained 1 week later during recovery.

MY Thoughts on ECGs #3,4,5,6:

The final 4 tracings in this case report were all recorded ~1 week later, as the patient was recovering. (Note that ECGs #3,4,5 are recorded at double standardization — while ECG #6 is recorded at normal standardization).

• The "good news" — is that overall the patient is improving clinically! That said — the rhythm remains chaotic. There definitely are periods of bradycardia (for which temporary pacing may be needed). There is an underlying sinus rhythm — with the “theme” being that there are lots of ectopics, including many different PAC shapes (therefore multiple PAC sites) and some PVCs.
• Overall — I think this rhythm “acts” like MAT. By strict definition — each P wave should change in shape with “true MAT” — and that does not quite happen, since there are periods of sinus rhythm. But as mentioned earlier — there is a “spectrum” of supraventricular arrhythmias — and sinus rhythm with lots of different looking PACs as we see here “acts” clinically like MAT. This type of rhythm may be seen with a very “sick” patient (as is the case here) — and/or with hypoxemia, electrolyte disorders, heart failure.
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• BOTTOM Line: It’s hard to be sure of every single beat on these rhythm strips — but determination of what each beat is, is not important. Instead — it is the “theme” that counts — which as I describe above, seems to be a highly variable series of arrhythmias that act clinically like MAT + PVCs — for which best treatment is support and a goal of optimizing treatment of this patient's heart failure (with possible component of acute myocarditis).

ECG #3:

• There is marked sinus bradycardia and arrhythmia. 
• Beat #4 is a PAC (Note that the P looks different in leads III and aVL). 
• Beat #5 is junctional escape (the sinus P in front of beat 5 has a PR too short to conduct!)

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ECG #4:

Figure-4: ECG #4 — obtained 1 week later during recovery.

ECG #4:

• Beats #1 and 2 are sinus conducted.
• Beats #3 and 6 look like PVCs. 
• Since the QRS is different and we see retrograde P waves — I think beats #4,5,9,11,13,15,17 are PVCs. 
• The other beats are PACs with different-looking P waves. 
• The fixed coupling for beats #4,5,9,11,13,15,17 supports these being PVCs.

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ECG #5:

Figure-5:  ECG #5 — obtained 1 week later during recovery.

ECG #5:

• Now that we know that the pointed P waves in lead II are the sinus beats — we can identify the P waves in front of beats #2, 6,7,8,9 as being sinus P waves. 
• Once again — the P in front of #6 is too short to conduct, so this is junctional escape. 
• After beat #9 — we see ventricular bigeminy with retrograde P waves (albeit with changing P wave morphology in front of supraventricular beats #11,13,15).

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ECG #6:

Figure-6: ECG-6 — obtained 1 week later during recovery.

ECG #6: 

• The first 6 beats show sinus bradycardia.
• I cannot tell for certain if the “dip” under the BLUE line is a PAC that then conducts with aberration — or if the last beat is a PVC.

 

ECG Blog #447 — A "Prophetic" P Wave ...

I was sent the ECG shown in Figure-1 — being told only that providers on the case suspected AFib (Atrial Fibrillation) with RBBB (Right Bundle Branch Block) aberrancy.

QUESTIONS:

• Is the wide tachycardia that is seen best in the chest leads, too irregular to be VT (Ventricular Tachycardia)?
•    — How certain are YOU of your answer?

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

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PEARL #1: Before reviewing my approach to today's challenging arrhythmia — it's important to clarify a commonly misunderstood concept: Although monomorphic VT is usually a regular (or at least almost regular) rhythm — it is not always regular!

• As reviewed in ECG Blog #231 — QRS morphology in VT may manifest a number of different forms. These include: i) Monomorphic VT — in which there is a similar (if not identical) QRS appearance throughout the episode of VT; ii) Polymorphic VT (PMVT) — in which QRS morphology continually changes from 1 beat-to-the-next (and which when associated with a long QTc interval — is known as Torsades de Pointes); and, iii) Several VT forms that are much less common in practice (ie, Pleomorphic VT — Bidirectional VT).
• 
  
• As noted in ECG Blog #444 — Reasons why monomorphic VT may not be regular include: i) There may be a "warm-up" period of slower and gradually accelerating ventricular beats before the VT becomes regularized; ii) There may be a "cool-down" period in which after the regular run of VT, the rate of VT progressively slows until the VT run finally resolves (these concepts thoroughly illustrated and explained in ECG Blog #417); and, iii) There may be more than a single VT reentry circuit sharing the same exit pathway — and/or the speed of conduction over the reentry circuit may vary (Oreto et al — Am Heart J 124(6):1506-11, 1992).

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MY Thoughts on the Rhythm in Figure-1:

The format used to record today's ECG provides a continuous rhythm strip recording that shows 21 consecutive beats. As seen in Figure-1 — the first 9 beats are displayed in each of the simultaneously-recorded limb leads — with the last 12 beats displayed in each of the simultaneously-recorded chest leads.

• PEARL #2: When confronted with a number of different ECG features on a single rhythm strip — I favor starting with the easier part(s) of the tracing. I save for last those parts of the tracing that are more difficult to interpret.
• Therefore — I began my interpretation by first identifying the 3 consecutive sinus-conducted beats ( = beats #6,7,8).
• Note that I placed colored arrows over the initial part of these sinus P waves in leads I and II (See Figure-2). And note that a precisely on-time 4th arrow appears just before beat #9. 
• KEY Point: It is the presence of this 4th precisely-on-time P wave that solves today's arrhythmia — because before we see the end of this 4th P wave, the rhythm is interrupted by a run of wide beats that continues until the end of this tracing!
• Note the 2 vertical dotted BLUE lines that I have added to Figure-2. These dotted lines mark the beginning of the QRS complex for beats #4 and #9 in each of the simultaneously-recorded limb leads. My purpose in drawing these dotted lines — is to show that in lead I, the initial part of the QRS complex for beats #4 and #9 is isoelectric and falls on the baseline.
• Focusing our attention now on lead I — it should be apparent that the 4th on-time RED arrow clearly occurs before the QRS of beat #4 — and that there clearly is not enough time for this 4th P wave to conduct to the ventricles. This defines the presence of AV Dissociation — which proves that beat #4 must be of ventricular etiology (ie, something "else" other than a sinus-conducted beat, must have occurred to produce widened beat #9). For more on the diagnostic significance of identifying AV dissociation in wide tachycardia — See ECG Blog #133 and ECG Blog #151.
• Since the presence of AV dissociation proves that beat #9 is of ventricular etiology — all other beats in Figure-2 that look the same as beat #9 must also be of ventricular etiology ( = beats #1-thru-5). And, since the run of consecutive wide beats that begins with beat #9 continues after the lead switch (that marks the change from limb leads to chest leads) — this run of VT (that begins with beat #9) continues throughout the rest of this rhythm strip!
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• PEARL #3: In addition to AV Dissociation — there are 2 additional features regarding QRS morphology of the wide beats in Figure-2 that prove the runs of wide beats represent VT. These are: i) Extreme axis deviation (since the QRS in lead I is all negative); — and, ii) Positive QRS concordance in all 6 chest leads (ie, When the QRS is either all positive or all negative in all 6 chest leads — this is virtually 100% predictive of VT).

BOTTOM Line: Today's case provides the best example I have seen that shows how monomorphic VT may sometimes be surprisingly irregular throughout its entire duration.

Figure-2: I've labeled P waves in the initial ECG. Note how irregular the run of VT that begins with beat #9 is, throughout its entire duration! 

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Acknowledgment: My appreciation to Javed Iqbal (from Leiah, Punjab, Pakistan) for the case and these tracings.

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ADDENDUM (9/13/2024): 

• I've reproduced below from ECG Blog #196 — a number of helpful figures and my Audio Pearl on assessment of the regular WCT rhythm.

 

Figure-5 : My LIST #1 = Causes of a Regular WCT (Wide-Complex Tachycardia) of uncertain Etiology (ie, when there is no clear sign of sinus P waves).

Figure-6: Use of the "3-Simple Rules" for distinction between SVT vs VT.

Figure-7: Use of Lead V1 for assessing QRS morphology during a WCT rhythm.

—  —

ECG Media PEARL #13a (12:20 minutes Audio) — reviews “My Take” on assessing the regular WCT (Wide-Complex Tachycardia), when sinus P waves are absent — with tips to distinguish between VT vs SVT with either preexisting BBB or aberrant conduction.

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Additional Relevant 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.
• ECG Blog #210 — Reviews the Every-Other-Beat (or Every-Third-Beat) Method for estimation of fast heart rates — and discusses another case of a regular WCT rhythm. 
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• ECG Blog #220 — Review of the approach to the regular WCT ( = Wide-Complex Tachycardia).
• ECG Blog #196 — Another Case with a regular WCT rhythm.
• ECG Blog #263 and Blog #283 and Blog #361 — more WCTs.
• ECG Blog #444 — a monomorphic VT rhythm that is not regular.
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• ECG Blog #197 — Reviews the concept of Idiopathic VT, of which Fascicular VT is one of the 2 most common types. 
• ECG Blog #346 — Reviews a case of LVOT VT (a less common idiopathic form of VT).
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• ECG Blog #204 — Reviews the ECG diagnosis of the Bundle Branch Blocks (RBBB/LBBB/IVCD). 
• ECG Blog #203 — Reviews ECG diagnosis of Axis, the Hemiblocks — and  the Bifascicular Blocks.
• ECG Blog #211 — WHY does Aberrant Conduction occur?
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• ECG Blog #42 — Review of criteria to distinguish between VT vs Aberration.

• Working through a case of a regular WCT Rhythm in this 80-something woman — See My Comment in the May 5, 2020 post on Dr. Smith’s ECG Blog. 
• Another case of a regular WCT Rhythm in a 60-something woman — See My Comment at the bottom of the page in the April 15, 2020 post on Dr. Smith’s ECG Blog. 
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• Review of the Idiopathic VTs (ie, Fascicular VT; RVOT and LVOT VT) — See My Comment at the bottom of the page in the September 7, 2020 post on Dr. Smith’s ECG Blog.
• Review of a different kind of VT (Pleomorphic VT) — See My Comment in the June 1, 2020 post on Dr. Smith’s ECG Blog (as well as ECG Blog #231).