EXTRA COPY — ECG Blog #539: Does SVT cause Hypotension? — EXTRA COPY

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The ECG in Figure-1 was obtained from a young adult woman — with a history of recurrent SVT. She was hypotensive with this most recent episode.

QUESTIONS:

• How would you interpret the ECG in Figure-1?
• Does this tracing "fit" with this patient's history?
• Extra Credit: Is there evidence of underlying atrial activity?

Figure-1: The initial ECG in today's case — obtained from a young adult woman with a history of recurrent SVT. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on this CASE:

The ECG in Figure-1 shows a regular WCT (Wide-Complex Tachycardia) at ~180-190/minute.

• Although in a number of limb leads the QRS does not seem wide — it "looks" wide in most of the chest leads, and measures 0.11-0.12 second in leads V1,V2.
• PEARL #1: I've seen different answers for what constitutes "QRS widening" in an adult. I favor the following 2 guidelines: i) For measuring QRS duration — Use that lead in which you can clearly determine the onset and offset of the QRS complex —  and in which the QRS is longest; — and, ii) Because some cases of fascicular VT may only measure 0.11 second in duration — I consider the QRS to be "wide" if in any lead it clearly measures ≥0.11 second in duration.
• PEARL #2: Just because a given diagnosis is written in a patient's chart — does not necessarily mean that diagnosis was correct (unless you also find firm objective evidence in that patient's chart to support the diagnosis!).
• PEARL #3: It is still all-too-commonly believed that the cause of the overwhelming majority of regular WCT rhythms in younger adults is some form of SVT (SupraVentricular Tachycardia) — in which QRS widening is explained by either preexisting BBB (Bundle Branch Block) or aberrant conduction. However, as was shown in ECG Blog #489 — and — Blog #38 — and — Blog #464, among others — the idiopathic VTs (which occur in patients without underlying heart disease) are much more common in younger adults than is currently appreciated (More on the idiopathic VTs below in today's ADDENDUM).

PEARL #4: Today's patient was hypotensive in association with the rhythm in Figure-1. Although it clearly is more common for a patient in VT to be hypotensive (than for a patient in an SVT rhythm) — a patient's BP (blood pressure) is not an infallible predictor for distinguishing between VT vs SVT (See ECG Blog #220 — Blog #38 — and — Blog #297).

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Because the QRS is wide in Figure-1 — We need to consider VT, as well as some form of SVT with either preexisting BBB or aberrant conduction. 

• PEARL #4: Aberrant conduction most often presents as rate-related QRS widening that manifests a QRS morphology that resembles some form of known conduction defect (ie, either RBBB, LBBB, LAHB, LPHB, or RBBB with a hemiblock). This is because the refractory periods of the various conduction fascicles are not the same. In most patients — the refractory period of the right bundle branch tends to be the longest, which is why RBBB conduction is the most common form of rate-related aberrancy. But any conduction pattern may be possible with rate-related aberrancy (See ECG Blog #211 — for more on the WHY of aberrant conduction).
• PEARL #5: As discussed in Figure-4 — fascicular VT is one of the most common forms of idiopathic VT. Because of its origin near the left anterior or the left posterior hemifascicle — QRS morphology with fascicular VT resembles either RBBB/LAHB or RBBB/LPHB conduction. That said — my favorite clue that a WCT rhythm may turn out to be fascicular VT — is that there are some atypical ECG features of RBBB conduction!

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Acknowledgment: My appreciation to Hamdallah Naser (from AL-Najaf, Iraq) — for allowing me to use this case and this tracing.

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ADDENDUM:

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• In Figure-9 — I review QRS morphology in lead V1 that suggests aberrant conduction.
• In Figure-10 — I summarize KEY features regarding idiopathic VT.

Figure-9: QRS morphology in lead V1 that suggests aberrant conduction vs VT (from my ACLS Pocket Brain-2013).

Figure-10: Review of KEY features regarding Idiopathic VT (See text).

—  —

ECG Media PEARL #14 (8 minutes Audio) — What is Idiopathic VT? — WHY do we care? Special attention to the 2 most common forms = RVOT (Right Ventricular Outflow Track) VT and Fascicular VT. 

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The CASE:

HI Sir. 19 year old girl with recurrent attack of palpitations and always with hypotension, treated with DC. Now presented again with same feature with undetected BP 

QUESTIONS — 1st is this AVNRT — andnd is it usual to cause hypotension ?

MY REPLY:

This is an absolutely beautiful case of Fascicular VT that looks like AVNRT — but we have PROOF that it is VT. The KEY is to note the changes in the baseline (best seen in lead II) — which as shown by the RED and PINK arrows represents AV Dissociation. The patient has hypotension because this is VT! (Yes, it is possible, but would be unusual in an otherwise healthy 19yo to have hypotension with AVNRT).

 

What is unique about this tracing — is that the negative notching after the QRS IS indeed 1:1 retrograde P waves — but note that these retrograde P waves do NOT occur following the QRS complexes in which the PINK arrow "on-time" sinus P wave coincides with the QRS! That's because these "on time" sinus P waves that are "dissociated" prevent retrograde VA conduction at this moment, but not at any other moment. 

 

So I definitely want to use this for an ECG Blog! — Do I have your permission to do so? I will be happy to acknowledge you (Hamdallah Naser from AL-Najaf, Iraq) if you like — or the case could be anonymous. In any event — I'll let you know in  about a month or so when I publish this. I will draw a laddergram to clear up the confusion regarding retrograde P waves. 

 

Clinically — Use IV Verapamil to treat recurrences. Since the patient has had several episodes — BEST approach is EP referral for ablation! In the meantime — I'd use oral Verapamil to hopefully present more episodes. Let me know what happens! — :)

HAMDALLAH Reply:

Of course you can use it Sir.

This her ECG after 100 j synchronised DC.

About TWI in the inf lead and V6 my colleague said this the first time appear (no TWI in the previous times after return of sinus rhythm).

Also another point her family mentioned that she not responding to adenosine many time in the past and always responds to verapamil (when she has no hypotension in some attack). Best regards

 

MY REPLY:

 Thanks for your permission to use the case — and thanks for the follow-up. What you say about recurrent episodes that fail to respond to Adenosine, but responding to Verapamil is perfectly consistent with Fascicular VT!

 

Assuming this patient is asymptomatic — the T wave inversion is most probablly "Memory" that is common following cardioversion after a prolonged tachycardia. In a 19yo — this typically is benign, and should resolve within hours to 1-2 days.

 

Will you be able to refer the patient for EP testing and ablation?

 

THANKS again — :) Ken

 

CASE Conclusion — from Hamdallah:

Yes Sir it was referred to specialised centre for EP study.

Thank for detailed explanation.

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ECG Blog #489

https://ecg-interpretation.blogspot.com/2025/07/ecg-blog-489-wide-tachycardia-in-20yo.html

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• PEARL #2: There are some ECG features that may allow for near-100% certainty in diagnosis. These include AV dissociation, capture and fusion beats. That said — these definitive ECG feaures will rarely be present with faster WCT rhythms, which are the most difficult ones to assess (Although I always look for these definitive ECG features — it is unlikely that we will find them in today's regular WCT at 180/minute). The failure to see AV dissociation, capture or fusion beats does not help diagnostically if none of these signs are seen (These ECG signs only help if present).
• PEARL #3: On occasion — Availability of a prior ECG may prove invaluable for ruling out VT by demonstrating an identical QRS morphology during sinus rhythm as was seen during the WCT rhythm. Unfortunately — it is rare that a prior ECG will be readily available at the time you are dealing with the WCT patient in front of you.
• PEARL #4: Hemodynamic stability during the WCT rhythm does not rule out VT. While true that patients with sustained VT are much more likely to decompensate than those who remain in a persistent SVT rhythm — these generalities do not always hold true. Some patients in sustained VT remain hemodynamically stable for hours — or even longer (with documentation of occasional cases of sustained VT having persisted for days — with providers around the bedside refusing to believe this to be possible). Therefore — hemodynamic stability can not be used to rule out VT.

What About Today's CASE?

As stated — today's patient is a previously healthy young adult with a history of "palpitations" — who presented to the ED hemodynamically stable in a regular WCT rhythm at 180/minute.

• Given this patient's young age and previously healthy status — ischemic VT is highly unlikely. But this patient could have idiopathic VT = the form of VT that is seen in ~10% of VT cases, in which VT occurs without any underlying heart disease (See Figure-4 in the Addendum below).
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• PEARL #5: Aberrant conduction most often presents as rate-related QRS widening that manifests a QRS morphology that resembles some form of known conduction defect (ie, either RBBB, LBBB, LAHB, LPHB, or RBBB with a hemiblock). This is because the refractory periods of the various conduction fascicles are not the same. In most patients — the refractory period of the right bundle branch tends to be the longest, which is why RBBB conduction is the most common form of rate-related aberrancy. But any conduction pattern may be possible with rate-related aberrancy (See ECG Blog #211 — for more on the WHY of aberrant conduction).
• PEARL #6: As discussed in Figure-4 — fascicular VT is one of the most common forms of idiopathic VT. Because of its origin near the left anterior or the left posterior hemifascicle — QRS morphology with fascicular VT resembles either RBBB/LAHB or RBBB/LPHB conduction. That said — my favorite clue that a WCT rhythm may turn out to be fascicular VT — is that there are some atypical ECG features of RBBB conduction!

Aberrant QRS Morphology in Lead V1:

Although exceptions exist — one would expect rate-related RBBB aberrancy to manifest a typical QRS morphology given that today's patient is an otherwise healthy young adult. In contrast — aberrant RBBB conduction in an older adult with underlying heart disease would be more likely to manifest a less typical QRS morphology (ie, "scar" from ischemic heart disease and/or cardiomyopathy being more likely to alter QRS morphology).

• As shown in the upper right insert in Figure-2 (and as is discussed in more detail in Figure-3 from the Addendum below) — typical RBBB conduction manifests a characteristic pattern in the 3 KEY leads that I rely on for recognition of the Bundle Branch Blocks (See ECG Blog #204 — for my user-friendly approach to diagnosis of BBB and IVCD within seconds!).
• With typical RBBB conduction — there is a distinct triphasic rsR' complex in right-sided lead V1 (with taller right rabbit ear — and S wave that descends below the baseline — consistent with A or B in Figure-2).
• The other characteristic feature of RBBB conduction — is the presence of wide terminal S waves in left-sided leads I and V6.
• PEARL #7: For practical purposes — the only QRS morphology with high specificity for SVT is the presence of the above described morphology (as shown in A or B in Figure-2). Although there are exceptions — any other QRS morphology (ie, C,D,E,F in Figure-2) favors VT.

Figure-2: QRS morphology is not quite "typical" for RBBB aberration.

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ANSWER: Applying QRS Morphology to Today's CASE:

I immediately thought ECG #1 in today's case was most likely to represent left posterior Fascicular VT.

• Although the widened, predominantly positive complex in lead V1 resembles RBBB conduction — QRS morphology in lead V1 is clearly more atypical than I'd expect for RBBB conduction in an otherwise healthy young adult. This is because instead of the expected triphasic QRS in lead V1 — we see an initial q wave with a slurred predominant R wave that manifests a taller left 'rabbit ear' (that most resembles pattern F in the insert in Figure-2).
• A similar qR pattern is seen in lead V2 — such that we never see any triphasic pattern.
• Wide terminal S waves are seen in left-sided leads I and V6 — but the QRS in the 3rd left-sided lead aVL looks very different than the QRS in lead I, and totally lacks a terminal S wave. Otherwise — QRS morphology in the inferior leads is perfectly consistent with LAHB conduction.

BOTTOM Line: Primarily on the basis of the very atypical QRS morphology in lead V1 in this otherwise healthy young adult — I thought QRS morphology to be most consistent with fascicular VT.

• PEARL #8: As discussed in Figure-4 — IV Verapamil is the treatment of choice for fascicular VT. The "beauty" of using IV Verapamil for this indication — is that this drug is also effective for treating the vast majority of reentry SVT rhythms, such that there is little downside to using IV Verapamil for treatment of today's WCT rhythm.
• NOTE: The caution with regard to using IV Verapamil or IV Diltiazem to treat a regular WCT rhythm — is that if the rhythm turns out to be an ischemic VT, that the vasodilating and negative inotropic action of these medications may precipitate deterioration of ischemic VT to VFib. That said — the previously healthy young adult in today's case is highly unlikely to have ischemic VT.

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CASE Follow-Up.

• The patient in today's case was initially treated with IV Adenosine. This was unsuccessful.
• IV Verapamil was then tried — and successfully converted the WCT to sinus rhythm.
• The patient was referred to EP Cardiology for consideration of ablation of her recurrent fascicular VT.

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EXTRA COPY — ECG Blog #536 — Why 2 Morphologies? — EXTRA COPY

The ECG in Figure-1 was sent to me for my thoughts. Initially I had no clinical information.

QUESTIONS:

• What is the rhythm?  
• Why are there 2 different QRS morphologies?
• What is the likely underlying cause of this rhythm?

Figure-1: The initial ECG in today's case — initially sent to me without clinical information. (To improve visualization — I've digitized the original ECG using PMcardio).

My Thoughts:

The overall rhythm in Figure-1 appears to be regular with obvious QRS widening — and a ventricular rate of just under 100/minute (ie, with an R-R interval just over 3 large boxes in duration).

• There are 2 different QRS morphologies.
• Although the R-R interval varies slightly — I attributed this to uncertainty regarding where the QRS begins in some leads.
• P waves are absent. The only suggestion of atrial activity that I saw is possible retrograde P waves in some chest leads.

PEARL #1: This tracing emphasizes the important concept that, "12 leads are Better than One" — because if you only looked at leads I and V1 (and/or at leads V2,V3,V4) — it would be easy to think the rhythm was simply AIVR (Accelerated IdioVentricular Rhythm). 

• Instead, as shown in Figure-2 — there clearly is an alternating QRS morphology that is seen every-other-beat.

Figure-2: For clarity — I've numbered the beats in the limb leads. 

What is Going On?

Based on what I saw in Figure-2 — I thought the following:

• There is a regular wide QRS rhythm at ~95/minute — but without clear sign of atrial activity. QRS morphology is not consistent with any known form of conduction block — so this most likelly represents a ventricular rhythm.
• Many leads strongly suggest that QRS morphology alternates every-other beat — but without explanation as to why this may be so (ie, There are no P waves that may be conducting — and no significant variation in R-R intervals that might be producing a rate-related effect).
• BOTTOM Line: I was left with the conclusion that the rhythm in Figure-2 most likely represents the rare arrhythmia known as BiDirectional VT.

Semantics:

I've previously reviewed the concept of "AIVR" (Accelerated IdioVentricular Rhythm) — which is a slower form of "VT" (See ECG Blog #108).

• Technically, AIVR is not "VT" — because the ventricular rate is not ≥100/minute. But the ventricular rhythm known as AIVR clearly is faster than the usual ventricular "escape" rate, which normally is between 20-40/minute ==> the designation preferred by many is that AIVR represents a form of "slow VT".
• As emphasized in Blog #108 — the importance of recognizing AIVR depends on the clinical setting in which it occurs (ie, AIVR often occurs as a reperfusion arrhythmia in patients who have had a recent MI).
• PEARL #2: Whenever I see AIVR — I carefully consider the possibility that the patient may have had a recent MI that could have passed undetected.

What is BiDirectional VT?

I presented a case of bidirectional VT in ECG Blog #436:

• As discussed in ECG Blog #231 — bidirectional VT is a special form of VT, in which there is beat-to-beat alternation of the QRS axis. This unique and very uncommon form of VT is distinguished from PMVT (PolyMorphic VT) and from pleomorphic VT — because a consistent pattern of alternating QRS morphology is seen every-other-beat throughout the VT episode.
• Typically with bidirectional VT — there are alternating longer-then-shorter R-R intervals that correspond to the alternating QRS morphology. That said — as was seen with the case I presented in ECG Blog #436 (as well as with today's case) — QRS widening with uncertainty in some leads as to where the onset of the QRS begins may render it difficult to distinguish subtle alternation in R-R interval duration from what otherwise appears to be a fairly regular ventricular rhythm.
• Technically — this raises the question as to whether today's rhythm might simply represent AIVR with alternating exit sites accounting for the alternating QRS morphology (as I allude to in my discussion of ECG Blog #231). While fully acknowledging these theoretical considerations — My impression of today's rhythm remains unchanged = the most likely explanation for the rhythm in Figure-1 is bidirectional VT.

PEARL #3: There are a limited number of causes of bidirectional VT. As reviewed by Almarzuqi et al (Vasc Health Risk Mgmt 18:397-406, 2022) — Potential Causes of Bidirectional VT include:

• Digitalis toxicity.
• CPVT (Catecholaminergic PolyMorphic VT).
• Acute myocardial ischemia.
• Familial hypokalemic periodic paralysis.
• Cardiac Sarcoidosis.
• Primary Cardiac Tumors and/or Cardiac Metastasis.
• Andersen-Tawil Syndrome ( = Long QT Syndrome, Type 7).
• Acute Myocarditis.
• Certain drug overdoses (Aconitine poisoning, severe caffeine poisoning).

PEARL #4: Given how rare bidirectional VT is — the 1st thing to do when contemplating this diagnosis is to consider whether the patient might have one of the above-listed potential causes of this rhythm.

• In years past — Digitalis toxicity used to be the most common cause of bidirectional VT. This no longer appears to be true — given the overall reduced use of Digoxin (and in those cases in which Digoxin is still prescribed — toxicity is much less common nowadays because dosing of this drug is so much less than it used to be). 
• With the exception of myocardial ischemia and myocarditis — the other entities listed as potential causes of bidirectional VT are rare (which explains why bidirectional VT is rare).
• To Emphasize: In my experience — bidirectional VT is not a common manifestation of myocardial ischemia. But the PEARL is that ischemia/infarction should always be considered whenever you contemplate a diagnosis of bidirectional VT.
• Clinically: The BEST treatment of bidirectional VT — is to identify the causative condition in the hope that there may be effective treatment of that condition.

Follow-Up in Today's CASE:

It turns out that today's patient was a previously healthy middle-aged woman — who presented to the ED (Emergency Department) with new-onset CP (Chest Pain). The patient's condition rapidly deteriorated with resultant cardiac arrest.

• A complicated course followed, fortunately with successful ROSC (Return Of Spontaneous Circulation) — and, at the earliest opportunity cardiac catheterization was performed.

QUESTION:

• What do you think cardiac cath showed?  

HINT #1: To facilitate assessment of QRST morphology for the 2 "families" of QRS complexes — in Figure-3, I've enclosed beat #3 and beat #6 within the BLUE and RED dotted rectangles. 

Figure-3: To facilitate assessment of QRST morphology — I've enclosed beats #3 and #6 within BLUE and RED dotted rectangles.

HINT #2: To facilitate concentration on ST-T wave morphology even more for the 2 "families" of QRS complexes — I've shaded out the remaining beats in the limb leads.

Figure-4: I've shaded out the remaining limb lead beats.

Answer:

Today's rhythm is bidirectional VT. This means that there are no normally conducted QRS complexes — but instead, all beats on today's tracing are ventricular in etiology.

• PEARL #5: Most acute OMI (Occlusion-based MI) tracings identified by ECG will be diagnosed on the basis of ST-T wave morphology changes in sinus-conducted beats. Assessment of ST-T wave morphology in PVCs is usually not a reliable indicator of an acute event.
• That said — On occasion, the shape of ST-T wave elevation or depression in one or more PVCs may be diagnostic of acute infarction. This is precisely what we for the PVCs in ECG Blog #359.
• NOTE: For an example of a case in which assessment of the normal (sinus-conducted) beats was not definitive for acute OMI — such that the diagnosis of acute infarction was only made by recognizing the abnormal ST-T wave morphology of several PVCs — See My Comment at the bottom of the October 8, 2018 post in Dr. Smith's ECG Blog.

Applying the advanced concept from PEARL #5 to today's tracing — the shape of ST-T wave morphology in Figure-5 is clearly disproportionate and "off" from what we'd expect for both QRS families. Specifically:

• The QRS family of odd beats in Figure-5 (illustrated by beat #3) — shows inappropriate ST elevation in the inferior leads with reciprocal ST depression in lead aVL (the RED and BLUE arrows in these leads).
• More subtle, but still evident — the QRS family of even beats (illustrated by beat #6) — shows inappropriate ST elevation in each of the inferior leads (which is especially apparent in lead II given tiny size of the QRS in this lead).
• Both families of QRS complexes show a disproportionately increased amount of ST depression in the mid-chest leads of Figure-5 — with the BLUE arrows in leads V2,V3,V4,V5 of the even-numbered beats highlighting the obvious abnormality of this finding by the marked amount of horizontal (ledge-like) ST depression.

CASE Conclusion: 

Today's ECG illustrates a case of bidirectional VT that developed as a result of acute infero-postero OMI. This was confirmed on cardiac catheterization that showed multi-vessel disease with acute total occlusion of the LCx (Left Circumflex) coronary artery.

Figure-5: Both families of QRS complexes suggest that the cause of this bidirectional VT is acute infero-postero OMI. 

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Acknowledgment: My appreciation to Fardeen Baray and Hameedullah Ahmadzai (from Kabul, Afghanistan) for the case and these tracings.

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EXTRA COPY — ECG Blog #535: A "Fluttering" ECG - EXTRA COPY

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

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Figure-2: XXXXX 

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Acknowledgment: My appreciation to Cardiology Notes (FB ECG site) for allowing me to use this tracing — and to Ahmed Marai (from Anbar, Iraq) for drawing my attention to this case.

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From Ahmed:

Hello Dr. Grauer — I came across this ECG on facebook, which belongs to to a 50-year-old male, hypertensive and diabetic, recorded while he underwent a routine check up.

This is the link to the poster

https://m.facebook.com/story.php?story_fbid=pfbid0wAJTSLDFuYExamcgrFy3RaR1DzcE6xbef7jf77Pdzy8htmBamYTTG5EJNSM2H13zl&id=61563573262961

This is my interpretation:

A 12 lead ECG, unlabelled calibration and speed, but it looks standard.

Ventricular rate: around 62-66 bpm

Rhythm: regular narrow complex rhythm

Axis: within normal range

No obvious P waves, however, there are regular waves between the QRS complexes, which run at around 273bpm, it appears in all the 12 leads and looks much taller in the chest leads compared to the limb leads.

Regarding QRS complex, it is narrow, with very subtle irregularity. In the chest leads, the QRS is dominantly positive (no obvious S waves), and has high voltage in V2-V5.

 

No obvious ST-T changes, and the QT intervals cannot be determined accurately.

Clinical impression: The regular waves seen between the QRS complexes are probably flutter waves, it runs at around 273bpm, and since ventricles beat at around 66bpm, then it is probably AFlu with 4:1 AV conduction. However, these flutter waves are atypically tall in the chest leads.

The high voltage of R waves in chest leads, is suggestive of possible LVH, the history of hypertension may support the possibility of LVH. The S waves are are not obvious in chest leads, but they are possibly present but are cancelled on the paper by the tall flutter waves. 

However, artifact should be suspected and excluded.

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My thoughts: At the beginning I thought this is an obvious atrial flutter with 4:1 av conduction, however, when I noticed the size of flutter waves in the chest leads, I thought this is unusual. 

I saw many people in the comments say, Artifact !! 

If this was an artifact coming from one limb, then one of these leads ( I, II or III ) should be spared. If the artifact is coming from 2 limbs, then it should be chaotic and not regular like this one.

If this was an artifact, then it is probably coming from the patient torso, maybe the patient was dancing while recording the ECG. This may explain why these waves are taller in the chest leads compared to the limb leads, as they are closer to the torso. Excited to hear your ideas on this ECG — Ahmed

MY REPLY:

Hi. I basically AGREE with you!

I’ve attached what I wrote on the FB site.

I also wrote to Cardiology Notes, asking them for follow-up! (They have great cases — but often don’t tells us what happened unless specifically asked!

: ) Ken

P.S. Another clue should be looked for — which is whether the DISTANCE between the closest deflection and the QRS is equal !!! Be SURE to use your calipers when looking for this. Usually (although not always) — IF the ventricular rhythm is regular — then the distance between the closest deflection and the QRS should be THE SAME! If it is not — and if the R-R interval remains constant — then this implies that NONE of the deflections are conducting!

But in this case — there is a very slight-but-real difference in the “PR” interval across lead II ==> IF the R-R interval would stay precisely equal, then if this was Aflutter — it implies complete AV block (which is possible but not common).

So — We wonder if this patient has a tremor, or perhaps something going on in his chest …

CARDIOLOGY NOTES (on Facebook !!! )

Hello Prof Ken. It was ARTIFACT! The patient is diagnosed with drug-induced Parkinsonism !!!!

EXTRA COPY — ECG Blog #537 — What is the Rhythm? — EXTRA COPY

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

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Figure-2: XXXX

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Figure-3: XXXX

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Figure-4: XXXX

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Figure-5: XXXX

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Acknowledgment: My appreciation to Bashiruddin Sayeem  (from Chittagong, Bangladesh) for the case and this tracing.

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THE CASE: Dear sir, this is an EKG of a 60 years old diabetic lady presenting with SOB. Is this LVH with strain, LAHB, RBBB?

MY REPLY:

Hello Bashiruddin — This is AIVR (or "or slow VT") at ~120/minute!

 

The KEY is to look at the long lead II — and RED arrows show 2 places were we KNOW there are 2 consecutive P waves (which are upright in this long lead II, therefore 2 consecutive sinus P waves. Now set your calipers at this P-P interval (between 2 consecutive RED arrows — and the PINK arrows show partial deflections that we SEE, which we KNOW must be underlying "on time" sinus P waves. The WHITE arrows then show you where additional "on time" sinus P waves lie — telling us there is an underlying sinus tach.

 

Thus there is AV dissociation — with beat #17 being a CAPTURE beat — and beats #6,7 and 16 being FUSION beats — all of which proves that the underlying rhythm is an isorhythmic AV dissociation by "usurpation" by an AIVR at 120/minute that is slightly faster than the underlying sinus tach! (The upright R wave in V1 is not "RBBB" — but indication of the ventricular focus!)

 

Note that the QRS IS actually wide (The tracing is slanted — but the WHITE line that I drew parallel to the heavy grid line shows that what looks like "narrow" beats in the long lead II are actually WIDE (because there is an initial small, upright r wave before the deep S waves)

 

Within the dotted BLUE rectangle we see the capture beat — that shows marked LVH with very deep, symmetric (ischemic) T wave inversion in leads V5,V6 — and also in lead aVF. That said, I don't acute ST elevation in the leads in which I am able to assess — so from what I can see, probably no acute STEMI ...

 

Now this 60 yo woman presented with SOB — so the KEY is to find out WHY she is SOB (ie, heart failure, pneumonia) — and then to treat that — and possibly (hopefully) the underlying "slow VT" will resolve!

 

This would be a SUPERB CASE for an ECG Blog! May I have your permission to use this case! I will acknowledge you as I have in the past (See attached). Let me know what happens! BEST — :) Ken

 

Bashiruddin REPLY:

Thank you sir Please feel free to use it in your ECG Blog.