Written by Magnus Nossen
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Hi Magnus — I recognize this case that you texted to me a little while back. The case IS a good one — but in my opinion, there is work to be done with the Figures (and with your description of the Figures). I've spent a few hours reviewing. My specific comments below. But first some general ones.
- You KNOW I am totally supportive of Cabrera format — and especially of familiarizing Blog readers with this (and other) formats. That said — I'll guess that 90+% of Blog readers do not encounter Cabrera format often. Most also are probably much more familiar with 25 mm/sec speed. Therefore — my suggestion is that you always reread your text with that type of reader in mind ... (I fully acknowledge that on the presentation ECG below — I have NO idea of what is going on because I think ( ??? ) that it is recorded at 50 mm/sec. speed — and my "brain" just doesn't "work" until I reduce width by 50%. And, since this is the KEY 1st tracing in your Blog post, my suggestion is that it is FINE to show this tracing first as is (specifying that the speed is 50 mm/sec).
- BUT — I would then ALSO post this same 1st ECG at 25 mm/sec.
- I think it is especially important to clearly indicate recording speed ON each ECG (especially since you have some 25 mm/sec tracings and some at 50 mm/sec).
- In my opinion — ALL Figures should always be labeled ON the actual ECG. My reasons for saying this are: i) It is otherwise confusing to me in places of your text which tracing you are talking about; and ii) When readers click on Figures to magnify them — especially in your cases where there are multiple Figures — it gets very confusing as to which Figure is which (because when clicked on to magnify — your legend does not show).
- MAGNUS — Below is the way I would write this up. Others do it differently — so I am merely offering my suggestions. It is UP TO YOU as to how you decide to do this.
- P.S. — Let me know if you need help with the Figures. If so — I'd need to have your best copy both in labeled (to orient me) and unlabeled form.
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The patient in today's case is a 80 something male with a medical history of hypertension and paroxysmal atrial fibrillation. He has been well controlled on flecainide therapy for many years. He presented to the emergency department due to syncope while at rest. Below in Figure-1 is the presentation ECG.
What do you think?
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| ECG #1 |
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| Figure-1: The initial ECG in today's case (recorded at 50 mm/sec). |
The above ECG is in the Cabrera format which is common in the Scandinavian countries. ECGs in the Cabrera format have been featured many times on Dr Smith's ECG blog. For an in-depth discussion on this ECG layout have a look at this blog post
For readers used to a 25 mm/sec. recording speed — I've reduced width by 50% (Figure-1a). Does this make it easier to interpret this tracing?
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| Figure-1a: The initial ECG in today's case (corrected to a recording speed of 25 mm/sec). |
The above ECG shows a regular rhythm with a QRS duration of about 120msec. The heart rate is approximately 100 beats per minute. There is a normal axis at 0 degrees. (Actually the frontal plane axis is about 0 degrees — given all pos in lead I but isoelectric in lead aVF. So of course a 0 degrees axis is "normal" — but it IS remarkable in being "different" than the usual axis. Problem could be easily solved by saying it's a normal axis at 0 degrees). There is no evidence of ischemia. (I'd start a new paragraph here) On questioning, the patient reported intermittent palpitations for the last few months. He was admitted to the hospital with a suspected diagnosis of sick sinus syndrome. ("With tachycardia" is not a new sentence — but rather a continuation from "sick sinus syndrome" ). With tachycardic spells (accounting for palpitations) and bradycardic spells likely being the cause of the recent syncope.
While on TM the following arrhythmia was captured: (Figure-2)
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| ECG #2 |
MAGNUS — This is the Figure I asked you about earlier. It is challenging to look at because: i) There is overlap in ALL chest leads, which I think (but really can not be certain) are pretty much all negative in all 6 leads; and ii) Lead V6 is cut off.
- I really think it important to acknowledge to your reader these challenges. If it were me — I probably would opt for a more readable tracing (ie, using 5 leads from aVL-to-aVF) — but it is FINE to show all 12 leads as you do IF you "comfort" the reader as to the problematic aspects. I'd do this by simply stating something like, "Unfortunately — there is overlap of the 5 chest leads that we see — and we have lost most of the lead V6 recording. That said — interpretation of this arrhythmia should still be possible".
This ECG shows a wide complex tachycardia with a heart rate of around 180 beats per minute. During the WCT the patient had a near syncopal episode. There was spontaneous termination? termination of WCT within approximately three minutes. The termination is shown below in Figure-3.
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| ECG #3 |
MAGNUS — I have no idea why you added the 2nd set of lead labels (within the dotted RED rectangle) — because this HIDES the actual "termination" of the rhythm.
What do you make of this clinical scenario? Do you agree that the WCT is ventricular tachycardia? What other possible explanations are there? Will you recommend ICD placement for this patient?
Discussion: I saw ECG number 1 by itself with the information that the patient was an elderly male on flecainide treatment presenting due to syncope. Instead, I'd phrase it more like this, "I initially saw the ECG in Figure-1, knowing only that the patient was an elderly man on flecainide, who presented to ED for syncope. I was told he had an episode of ventricular tachycardia. I was not convinced the WCT was ventricular in origin. Why did I think this? (this is the perfect place to use italics = Why did I think this? .
I'd leave a little space before you give the answer. To prevent a "spoiler" — just skip a few lines and add a heading in bold ...
MY Thoughts on the ECG in Figure-2:
Lead V1 in the initial ECG in todays case made me doubt the diagnosis of VT. Let us have a closer look at V1 from the presentation ECG. Below I have magnified leads V1-V2. Let's look closer at a magnifed view of leads V1 and V2 from today's initial tracing (Figure-4). The This ECG was interpreted as showing sinus tachycardia.
Remember! It would be very unlikely for an 80-something to have a resting sinus rate of 100bpm in the presence of negative chronotropic medication unless there is some underlying cause like infection, anemia, hypoxemia or other illness that leads to an increase in sympathetic tone.
What at first glance could be mistaken for sinus tachycardia is in fact not. There are deflections at the end of the QRS (best seen in V1). Below I have marked atrial activity with arrows.
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| Figure-4: Magnified view of leads V1,V2 from Figure-1. (Recording speed was 50 mm/sec.). |
In order to prove beyond any doubt that this is not sinus tachycardia but rather 2:1 atrial flutter, I went to the telemetry station and found the ECG below in Figure-5. ECG. This ECG shows a regular atrial arrhythmia with a cycle length in the atria of about 320msec. There is varying degree of AV block BEST not to refer to variable conduction with AFlutter as a form of "block" — because "block" implies pathology, and variable conduction with AFlutter is physiologic (and usually goes away if you convert the rhythm to sinus) with predominant 2:1 and sometimes 3:1 conduction. (So this is actually intermittent dual-level AV block with Wenckebach conduction out of the AV node. I can eventually draw a laddergram of this interesting rhythm. You could simplify your description by simply saying "there is AFlutter with predominant 2:1 AV conduction, with some variable conduction out of the AV node" ).
Magnus — since you have mixed recording speeds on today's tracings — for clarity I think it important ON the actually ECG to indicate the recording speed used for each tracing. This tracing did have it — but the writing was tiny and blurred. EASIEST approach — is WHITE OUT that writing — don't worry about the 10mm/mV — but write clearly, "25 mm/sec." — :)
Below is a magnified image of leads V1-V3 from the above ECG. There is 2:1 and 3:1 conduction with a fairly controlled ventricular rate. I'd DELETE this Figure — because: i) This magnified view is TOO SMALL to adequately assess conduction ratios; and ii) Rather than strict "3:1" — I suspect this is a variation of dual-level AV block with Wenckebach conduction out of the AV node — NOTE that the PR intervals in lead V1 toward the beginning of the Fig. 5 rhythm strip VARY! And with AFlutter, because of "concealed conduction" — it is usually NOT the closest flutter wave that conducts. I actually will eventually need an unhurried 30-60 minutes to "play" with this rhythm strip until I get it to "work out" — which I'll be happy to do when you're done with your revisions — :)
Let us go back to the WCT and have a closer look at the RR intervals before and after termination. Before termination, the R-R intervals of the WCT is about 360ms. As you can see there is a doubling of the R-R intervals from about 360msec to 720msec. This is consistent with 1:1 and then 2:1 conduction of atrial arrhythmia.
When the cycle length in atria prolongs this may lead to 1:1 conduction. The patient in today's case was not prescribed an AV nodal blocker, which is mandatory when treating atrial fibrillation and atrial flutter with flecainide. Patients need AV nodal blockers precisely to prevent what happened to this patient.
MAGNUS — I feel the above 2 paragraphs and construction of the figure shown here needs revision. The problems are that after beat #12 — the R-R interval is NOT regular (there is slight R-R interval variation, not only for the R-R interval between #12-13, but beyond that). Also — I am not convinced that after beat #12 that there is AFlutter ... (it could be AFib). Lead V5 is just not convincing to me of flutter waves (even going back to Fig. 1 when we have 2:1 clearly seen in lead V1 — I did NOT see convincing 2:1 atrial activity in lead V5 ...
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The QRS axis of the WCT in today's case is atypical for 1:1 atrial flutter as there are negative QRS complexes in the inferior leads. I didn't think AFlutter influenced what the QRS frontal plane axis had to be ... There are several possible causes of this. First sodium channel blocker and tachycardia may produce conductions disturbances. Note that the axis does not change after the rate drops. Beat #12 in WHICH Figure are you talking about here? is slightly wider than the other beats likely owing to some form of rate related conduction delay. Furthermore, the WCT was recorded via telemetry. The 12 lead ECG with the WCT and its termination is in fact a derived 12 lead from a five lead telemetry. It is not unlikely that telemetry leads were misplaced with may alter the QRS axis.
Conclusion: This is YOUR theory — but are you 1,000% certain? EASILY fixd by beginning by say, "I suspect that The wide complex tachycardia (WCT) was due to intermittent 1:1 conducted 1:1 AV conduction of atrial flutter. (MAGNUS — I'm a bit confused between what we think is rate-related aberrant conduction vs QRS widening produced by flecainide ...) atrial arrhythmia with aberrant conduction. Flecainide was discontinued and a betablocker was started. After the flecainide treatment was withdrawn the atrial cycle length I'm confused about what cycle length you are talking about? Is this the P-P interval? Might be much easier to conceptualize if you talk about the approximate change in atrial rate of the underlying AFlutter (ie, the atrial flutter rate went from ~300/minute to XXX/minute — whatever those rates which I have not calculated happened to be). shortened significantly and the patient despite betablocker treatment remained in a 2:1 conducted atrial flutter AFlutter with 2:1 AV conduct, with a ventricular response of at about 140 beats per minute. He was later cardioverted and referred for atrial flutter ablation.
Looks like you are summarizing ... — so I'd skip a few lines and add a brief heading ...
In Summary: The initial ECG in todays case was initially interpreted as showing sinus tachycardia. What made me this this was unlikely? There are three main reasons.
Clinical picture did not fit sinus tachycardia
All-upright P-waves in V1 does not occur in sinus rhythm An all-upright sinus P wave in lead V1 is not common (BUT IT CAN OCCUR!). In contrast — atrial morphology in lead V1 is perfectly consistent with AFlutter.
(but does occur with flutter!)
- Terminal portion of V1 had the look of «hidden» atrial activity. Much more than just "the look" of hidden atrial activity — IF you take your calipers — there is an IDENTALLY shaped notch right after the QRS in your magnified Figure-4. I was 99+% certain of 2:1 AFlutter as soon as I saw that — :)
2:1 flutter can sometimes be difficult to discern from sinus tachycardia. Always consider this arrhythmia if clinical picture does not fit with sinus tachycardia. MAGNUS — To me, we are really talking about the "Bix Rule" — in that the PR interval of a sinus rhythm typically shortens with tachycardia — yet the PR interval "looks long" in Figure-1 (I am unable to calculate the actual PR interval — but doing so would add to your discussion — since it is the "Bix Rule" that has tipped me off countless times that sinus tach is not present). IF interested — I review the BIX RULE in my ECG Blog #227 ( https://tinyurl.com/KG-Blog-227 )
Always consider Consider atrial flutter or atrial tachycardia if P wave is all-upright in V1.
- Flecainide may slow atrial flutter sufficiently to allow 1:1 AV conduction. Never prescribe flecainide without give av nodal blockers to patients with atrial fibrillation or atrial flutter.
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BELOW IS MAGNUS 12/28 DRAFT
Written by Magnus Nossen
The patient in today's case is a 80 something male with a medical history of hypertension and paroxysmal atrial fibrillation. He has been well controlled on flecainide therapy for many years. He presented to the emergency department due to syncope while at rest. Below is the presentation ECG.
What do you think?
|
| ECG #1 |
The above ECG is in the Cabrera format which is common in the Scandinavian countries. ECGs in the Cabrera format have been featured many times on Dr Smith's ECG blog. For an in-depth discussion on this ECG layout have a look at this blog post
The above ECG shows a regular rhythm with a QRS duration of about 120msec. The heart rate is approximately 100 beats per minute. There is a normal axis. There is no evidence of ischemia. On questioning, the patient reported intermittent palpitations for the last few months. He was admitted to the hospital with a suspected diagnosis of sick sinus syndrome. With tachycardic spells (accounting for palpitations) and bradycardic spells likely being the cause of the recent syncope.
While on TM the following arrhythmia was captured:
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| ECG #2 |
This ECG shows a wide complex tachycardia with a heart rate of around 180 beats per minute. During the WCT the patient had a near syncopal episode. There was termination of WCT within approximately three minutes. The termination is shown below.
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| ECG #3 |
What do you make of this clinical scenario? Do you agree that the WCT is ventricular tachycardia? What other possible explanations are there? Will you recommend ICD placement for this patient?
Discussion: I saw ECG number 1 by itself with the information that the patient was an elderly male on flecainide treatment presenting due to syncope. I was told he had an episode of ventricular tachycardia. I was not convinced the WCT was ventricular in origin. Why did I think this?
Lead V1 in the initial ECG in todays case made me doubt the diagnosis of VT, Let us have a closer look at V1 from the presentation ECG. Below I have magnified leads V1-V2. The ECG was interpreted as showing sinus tachycardia.
Remember! It would be very unlikely for an 80-something to have a resting sinus rate of 100bpm in the presence of negative chronotropic medication unless there is some underlying cause like infection, anemia, hypoxemia or other illness that leads to an increase in sympathetic tone.
What at first glance could be mistaken for sinus tachycardia is in fact not. There are deflections at the end of the QRS (best seen in V1). Below I have marked atrial activity with arrows.
In order to prove beyond any doubt that this is not sinus tachycardia but rather 2:1 atrial flutter, I went to the telemetry station and found the below ECG. This ECG shows a regular atrial arrhythmia with a cycle length in the atria of about 320msec. There is varying degree of AV block with predominant 2:1 and sometimes 3:1 conduction.
Below is a magnified image of leads V1-V3 from the above ECG. There is 2:1 and 3:1 conduction with a fairly controlled ventricular rate.
Let us go back to the WCT and have a closer look at the RR intervals before and after termination. Before termination, the R-R intervals of the WCT is about 360ms. As you can see there is a doubling of the R-R intervals from about 360msec to 720msec. This is consistent with 1:1 and then 2:1 conduction of atrial arrhythmia.
When the cycle length in atria prolongs this may lead to 1:1 conduction. The patient in today's case was not prescribed an AV nodal blocker, which is mandatory when treating atrial fibrillation and atrial flutter with flecainide. Patients need AV nodal blockers precisely to prevent what happened to this patient.
The QRS axis of the WCT in today's case is atypical for 1:1 atrial flutter as there are negative QRS complexes in the inferior leads. There are several possible causes of this. First sodium channel blocker and tachycardia may produce conductions disturbances. Note that the axis does not change after the rate drops. Beat #12 is slightly wider than the other beats likely owing to some form of rate related conduction delay. Furthermore, the WCT was recorded via telemetry. The 12 lead ECG with the WCT and its termination is in fact a derived 12 lead from a five lead telemetry. It is not unlikely that telemetry leads were misplaced with may alter the QRS axis.
Conclusion: The wide complex tachycardia (WCT) was due to intermittent 1:1 conducted atrial arrhythmia with aberrant conduction. Flecainide was discontinued and betablocker was started. After the flecainide treatment was withdrawn the atrial cycle length shortened significantly and the patient despite betablocker treatment remained in a 2:1 conducted atrial flutter at about 140 beats per minute. He was later cardioverted and referred for atrial flutter ablation.
The initial ECG in todays case was initially interpreted as showing sinus tachycardia. What made me this this was unlikely? There are three main reasons.
2:1 flutter can sometimes be difficult to discern from sinus tachycardia. Always consider this arrhythmia if clinical picture does not fit with sinus tachycardia.
Always consider flutter or atrial tachycardia if P wave is all-upright in V1.
- Flecainide may slow atrial flutter sufficiently to allow 1:1 AV conduction. Never prescribe flecainide without give av nodal blockers to patients with atrial fibrillation or atrial flutter.
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