- A) AFib with a rapid ventricular response.
- B) SVT with RBBB aberration.
- C) The rhythm could be VT.
- D) The rhythm is VT.
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| Figure-1: Which of the above choices is the best answer? = = = = = = = [ Abbreviations: AFib (Atrial Fibrillation) — SVT (SupraVentricular Tachycardia) — RBBB (Right Bundle Branch Block) — VT (Ventricular Tachycardia)]. |
- Take another LOOK at today's tracing in Figure-2. For clarity — I've numbered the beats in the long lead II rhythm strip.
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| Figure-2: I've numbered the beats in today's tracing. |
- The overall rhythm is Regular — at a Rate of ~150/minute (ie, with an R-R interval of ~2 large boxes in duration).
- The QRS is wide (at least 3 small boxes in duration — therefore ≥0.12 second).
- Are there P waves?
- The fact that the R-R interval in Figure-2 is regular effectively rules out AFib (If we can confirm that P waves are truly present — this would definitively rule out AFib).
- The rhythm in Figure-2 is a regular WCT (Wide Complex Tachycardia).
- The rate of the rhythm is ~150/minute.
- There is no clear sign of sinus P waves (ie, There is no consistent upright P wave with constant PR interval preceding each QRS complex in the long lead II rhythm strip).
- The above said — a number of small upright deflections in the baseline do appear to be present throughout the long lead II. These could be P waves.
- PEARL #1: Assuming today's patient is an adult — by far, the most common cause of a regular WCT rhythm without clear sign of sinus P waves is VT. Therefore — We need to assume VT until proven otherwise!
- Although the predominantly upright QRS complex in lead V1, in association with wide terminal S waves in lateral lead V6 could be consistent with RBBB conduction — you virtually never should see an all negative QRS complex in lead I with a supraventricular rhythm.
- Based on QRS morphology then — this strongly suggests that the rhythm in Figure-2 is VT (which means we can effectively rule out SVT with RBBB aberration).
- Are we 100% certain that today's rhythm is VT?
- IF we were at the bedside with this patient — the 1st thing we would do is determine if the patient is hemodynamically stable! That's because if the patient is not stable with this rhythm — then it would no longer matter what the rhythm is, because synchronized cardioversion would then be immediately indicated.
- NOTE: I've described my above thoughts in slow motion. With practice and experience — You should be able to arrive at this point in the process in no more than 10-to-15 seconds!
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| Figure-3: XXX |
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| Figure-4: XXX |
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| Figure-5: XXX |
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| Figure-6: XXX |
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| Figure-7: XXX |
ADDENDUM (2/XXX/2026):
I refer the reader to my ECG Blog #196 — in which I walk through a similar problem-solving process for another regular WCT rhythm.
- I've excerpted from that post my Audio PEARL on assessing the regular WCT — as well as Figures on my "3 Simple Rules" and on QRS morphology in lead V1.
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| Figure-8: Use of the “3 Simple Rules” for distinction between SVT vs VT (excerpted from my ACLS-2013-ePub). |
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| Figure-9: Use of lead V1 for assessing QRS morphology during a WCT rhythm (excerpted from my ACLS-2013-ePub). |
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Константин Тихонов <dropattack03@icloud.com> (2/11/2026)
I had a patient on call today. This is a 45-year-old man with a history of hypertrophic cardiomyopathy (without obstruction of the outflow tract of the left ventricle) and thyrotoxicosis. In January of this year, he had two similar episodes, and he was hospitalized twice by an ambulance team. Both times, the rhythm was restored with the help of electric pulse therapy. The diagnosis was ventricular tachycardia. He called an ambulance for a rapid heartbeat. During our examination, the patient was not pale, and there was no diaphoresis. His blood pressure was 125/70, compared to his normal blood pressure of 130/80. His oxygen saturation was 97%. His respiratory rate was 16.
ECG No. 1 was recorded first. After that, there was a short episode of sinus rhythm recovery with premature ventricular complexes, after which the tachycardia with wide QRS complexes recurred (ECG No. 2).
ECG No. 3 was recorded after 150 mg of amiodarone, after which the patient felt a significant improvement in his well-being.
My opinion:
I believe that ECG No. 1 shows ventricular tachycardia.
1. There is an almost regular rhythm with small differences in RR intervals in some places. (Black lines)
2. The electrical axis on ECG No. 1, in my opinion, is approximately +120 degrees, while on ECG No. 3 it is about +60 degrees.
3. I have marked with red arrows on ECG No. 1 the possible presence of atrioventricular dissociation, which I believe is present.
4. The R nadir time in lead II is more than 50 ms.
5. The QRS complexes in tachycardia are similar in morphology to the premature ventricular complexes on ECG No. 3.
ECG No. 3 raises special questions. It seems to me that there are regular P waves, the first of which are conducted, while the second are not and are hidden in the ST-T of the ventricular extrasystoles. These P waves are very similar in morphology to the sinus waves, as can be seen by comparing their morphology, which I have indicated with blue arrows on ECG No. 3. Also, these possible P's are not premature, so they are probably not blocked atrial extrasystoles. Is it possible that after a sinus contraction, a ventricular extrasystole occurs that retrogradely depolarizes the AV node, but the next sinus P finds the AV node in the absolute refractory period and is not conducted to the ventricles?
MY REPLY:
Hi Konstantin.Yes — VERY interesting case. I would like to do an ECG Blog on this case. Because the tracings are so long, I will need to reduce them — and I probably will only show the 1st and 3rd tracings together with the laddergram that I’ve drawn below. If OK by you — I will acknowledge you — and I’ll let you know when I publish this (it may be a little while — as I have other cases to go before this).
MUCH better to show this tracing when you ask the question about retrograde P waves — because I can now directly refer to this ECG.
- There are NO retrograde P waves. You did a GREAT job highlighting the P waves. There is often some underlying sinus arrhythmia — which is the reason for slight change in P-P intervals.
- You PROVE beyond doubt (100%) that this rhytm is VT. Assuming no lead misplacement — you virtually NEVER see an all negative QRS in lead I.
- You very nicely highlight the on-time sinus P waves. This establishes AV dissociation, which especially given the abnormal QRS morphology tells us 100% that this rhythm is VT.
- Your ECG #3 shows ventricular bigeminy. The attached laddergram shows what is happening = on-time sinus P waves that are unable to conduct because the ventricular beats do conduct retrograde and therefore prevent every-other on-time P wave from being conducted down to the ventricles.
- This is a NICE PEARL — the fact that on-time sinus P waves continue throughout the tracing proves that beats #2,4,6,8,10,12 can not possibly be supraventricular (because if they were supraventricular, they would have reset the SA node)
I hope this makes sense. You did a GREAT job mapping out the P waves and the AV dissociation — and this PROVES this rhythm is VT.
Do you have any more follow-up on this patient!
Take care.
: ) Ken
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KONSTANTIN Reply:
Thanks a lot, Ken. I am very glad that my version turned out to be correct, because I am now trying to learn to understand complex rhythms in more detail.
On account of this patient. Later that night, the patient called an ambulance twice more and had two more recurrences of ventricular tachycardia. As a result, he was admitted to the hospital. He has been assigned to conduct an electrophysiological examination and the issue of installing a cardioverter-defibrillator will be considered.
- How would YOU interpret this tracing?
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| Figure-1: 12-lead ECG obtained from a 40-year old man. He was hemodynamically stable at the time this ECG was recorded. |
- The rhythm is fast and regular (although not quite as fast as one might think from initial inspection = about 115/minute). The QRS is wide. Regular sinus P waves that conduct are not seen (ie, there is no upright P wave with constant and normal PR interval before each QRS complex in lead II).
- PEARL #1: As emphasized often on these ECG Bogs — the most common cause (by far!) of a regular WCT rhythm without sinus-conducting P waves is VT (Ventricular Tachycardia). Depending on clinical circumstances of the case at hand — between 80-to-90+% of such rhythms will turn out to be VT. For that reason — ALWAYS assume VT until proven otherwise!
- PEARL #2: Prominent among ECG features that may assist in the diagnosis of a regular WCT — is QRS morphology. VT is favored IF — QRS morphology does not resemble any known form of conduction defect (ie, LBBB or RBBB, with or without a hemiblock). This is the case with the ECG in Figure-1. Although the predominantly upright qR pattern in lead V1, with wide terminal S wave in lead V6 resembles RBBB (Right Bundle Branch Block) conduction in the chest leads — the indeterminate frontal plane axis (ie, leads I,II,III all predominantly negative) is not typical for RBBB conduction in the limb leads. That said — I thought QRS morphology in ECG #1 was clearly not definitive for a ventricular etiology.
- NOTE: For review of "My Take" on the ECG approach for assessing the regular WCT rhythm — Check out ECG Blog #196 — Blog #220 — Blog #263 — and Blog #283 —
- HINT: Take Another LOOK at the ECG in Figure-1. WHY might QRS morphology in lead II be changing?
- See Figure-2 ...
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| Figure-2: RED arrows highlight why QRS morphology in lead II is subtly changing (See text). |
- PEARL #3: The fact that the position of the 5 P waves highlighted by these RED arrows is constantly moving with respect to its neighboring QRS complex — tells us that these P waves are unrelated to QRS complexes (ie, there is complete AV dissociation for these 5 beats). This finding of complete AV dissociation of a regular atrial rhythm from the wide tachycardia (at least for a significant portion of the WCT rhythm) — is virtually diagnostic of VT (See ECG Blog #133 — Blog #134 — and Blog #151 for additional examples illustrating how AV dissociation allows you to confirm the diagnosis of VT!).
- PEARL #4: Although the ECG finding of AV dissociation provides invaluable assistance for confirming the diagnosis of VT — it will usually not be seen with the most problematic forms of VT (which are those VTs that occur at faster heart rates). This is because the faster the ventricular rate of VT — the more likely it is that underlying sinus P waves will be hidden (ie, within QRS complexes or within ST-T waves). It is because the ventricular rate of the WCT rhythm in today's case was relatively slow (ie, only ~115/minute) — that we are able to identify AV dissociation for the 5 P waves highlighted by RED arrows in Figure-2 (Note that we do not see evidence of AV dissociation in the rest of today's tracing).
- PEARL #5: In my experience — AV dissociation is greatly overdiagnosed! There is a tendency to label as "AV dissociation" any (and sometimes all) unexpected deflections seen in a WCT tracing. Most of the time (in my experience) — these "extra" deflections are not underlying P waves — but rather reflect artifact that is so common in symptomatic patients with marked tachycardia. Because of the clinical implications of identifying true AV dissociation in a regular WCT rhythm (ie, it virtually proves the rhythm is VT!) — I favor only diagnosing AV dissociation when you can be certain it is present (ie, when you can reliably identify at least a series of regular underlying P waves at a constant rate — as is possible for the 5 consecutive RED arrows seen in Figure-2).
- PEARL #6: As I've emphasized — the rate of the regular WCT rhythm in today's tracing is not fast. It is ~115/minute — which lies at the limit between a "slower" form of VT = AIVR (Accelerated IdioVentricular Rhythm — which is often benign and associated with reperfusion) — and a "faster" VT rhythm (with much higher risk of deterioration to VFib and cardiac arrest). As a result — the clinical significance of today's rhythm will depend on the patient's hemodynamic stability — and — on clinical factors such as whether this rhythm represents a positive (and transient) sign that reperfusion of the "culprit" artery has just occurred. KEY POINT: Depending on these factors — the risk of today's rhythm deteriorating to VFib and cardiac arrest might be limited — and cardioversion or antiarrhythmic treatment might not necessarily be needed (See ECG Blog #108 and Blog #125 for more on AIVR).
- In the absence of more clinical information — I'd consider optimal interpretation of today's rhythm = "Ventricular Tachycardia at a rate of 115/minute".
- I'd emphasize the need for clinical correlation to determine IF antiarrhythmic treatment, cardioversion — or — a "tincture of time" (ie, with no active treatment) is likely to represent the BEST approach to initial management.
Acknowledgment: My appreciation to Ahmed Shaaban (from Cairo, Egypt) for the case and this tracing.
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Related ECG Blog Posts to Today’s Case:
- ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
- ECG Blog #185 — Reviews my Systematic Approach to Rhythm Interpretation.
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