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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