-USE.png) |
| Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio). |
- How would you interpret the ECG in Figure-1?
- Do the wide beats represent NSVT (Non-Sustained Ventricular Tachycardia) — or aberrant conduction?
- How certain are you of your answer?
- What would you do?
- Does this ECG show anything else?
- This matches the clinical reality that we so often encounter — that is, seeing a patient for whom we need to initiate management before we know for certain what the diagnosis is.
- What are the hints in this tracing that either point to the likelihood of VT? — vs suggesting that the wide beats are aberrantly conducted?
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| Figure-2: I've numbered the beats in today's tracing. |
- Numbering the beats instantly allows better appreciation of the relationship between the elements of a complex tracing.
- It also allows you to intelligently discuss the case with others (Since otherwise, valuable time will inevitably be lost trying to figure out which beat(s) is being discussed).
- NOTE: We lack a long lead rhythm strip in today's case. If I was seeing this patient in real time — I would immediately record a period of ongoing monitoring in a long lead II, since otherwise there is no way to tell if the frequent changes in QRS shape are the result of a single QRS morphology or multiple QRS morphologies.
- To answer this question — I focused my attention on the narrow beats in Figure-2. These are beats #7,8,9; — 11,12,13; — 15,16,17; — 23,24,25.
- Note that no P waves are seen anywhere in Figure-2.
- Note also that the overall heart rate of the narrow beats in this tracing is fast — with a constantly changing R-R interval that is less than 3 large boxes in duration ( ==> the average ventricular rate is over 100/minute).
- Impression: The underlying rhythm in today's tracing, as suggested by the irregularly irregular narrow QRS complexes without P waves in Figure-2 — appears to be AFib (Atrial Fibrillation), here with a rapid ventricular response.
- Note that despite the underlying rhythm of AFib — the coupling interval of wide beats in this tracing remains the same! (ie, The distance from the narrow beat that precedes wide beats #10,14,18,26 is constant — as highlighted below by the 4 "C's" in Figure-3).
- Given that the underlying rhythm in today's tracing is AFib — Shouldn't we expect the coupling interval to be as irregular as the underlying rhythm? (In contrast, with premature ventricular beats — the reentry mechanism that is most often operative usually results in a constant coupling interval).
- In addition — a post-ectopic pause (labeled "P") occurs after the 2 short runs of wide beats in Figure-3 (and a post-ectopic pause is clearly more likely to be seen after a run of ventricular beats compared to aberrantly conducted beats when the rhythm is AFib — since a run of wide beats with aberration tends to maintain a similar degree of irregularity as the underlying AFib).
- Finally — QRS morphology for the wide beats in Figure-3 is atypical for LBBB conduction, in that a predominantly positive QRS complex is already seen by lead V3, whereas normally — transition in the chest leads (ie, the point where the R wave becomes taller than the S wave is deep) does not occur until lead V5 or V6 when there is LBBB conduction.
- NOTE: QRS widening in Figure-3 does not manifest the Ashman phenomenon. This is because with the Ashman phenomenon — QRS widening from aberrant conduction follows a longer pause that predisposes to subsequent aberrant conduction by lengthening the subsequent relative refractory period. This is not what we see before beats #10,14,18,26 (See ECG Blog #70 and ECG Blog #71 — for review of the Ashman phenomenon).
- From a statistical viewpoint — Intermittent QRS widening from aberrant conduction occurs more commonly than ventricular ectopy. That said — the combination constant coupling intervals, post-ectopic pauses after runs of wide beats, and a QRS morphology for the wide beats that is atypical for LBBB conduction — all favor ventricular ectopy as the cause of intermittent QRS widening.
- If the wide beats are of ventricular etiology — then the runs of 6 and then 5 consecutive wide beats ( = beats #1-thru-6 — and then #18-thru-22) constitute runs of NSVT. That said — since we do not see what happened before beat #1 in Figure-3 — We have no idea as to how long the 1st run of wide beats really lasts?
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| Figure-3: I’ve labeled findings suggestive |
- In the absence of more information (and a prior ECG) — We do not know if the AFib in today’s case is new or old? Presumably — the runs of NSVT are new. Therefore — We are speculating.
- Do you see any potential clues to the cause of the runs of NSVT in Figure-3?
- HINT: Look closely at ST-T waves in the chest leads …
- For assessment of ST-T wave morphology — it’s best to focus attention on the normally conducted ( = narrow) beats.
- ST-T waves in narrow beats #7,8,9; 11,12,13; and 15 — show nonspecific ST-T wave flattening.
- However, in the chest leads — there appears to be maximal ST depression in leads V3,V4,V5 (BLUE arrows in these leads)
-ST%20dep-post%20OMI-USE.png) |
| Figure-4: XXXX |
THE CASE (from Ahmed Abbas — Anonymous!
Dear Dr.Grauer. I hope you are doing well.
Today i present to you a case of a 49 year old woman,pre DM, presented to our urgent care center with dizziness and palpitations for the past 2 hours.
she denies and chest pain, shortness of breath , or syncope.
Her vitals were BP 118/63, sat 99 on RA, pulse 182.
Here ECG showed atrial fibrillation with runs of nonsustained Vtach,her troponin was negative , received 150mg of amiodarone then transported to hospital.
kindly help us interpreting the ECG with the details you usualy provide.
my questions:
1. were those runs of psvt or appatently conducted atrial fibrillation?
2. the widw complex qrs after narrow ,is it ashman?
3. what causes the re-entry if there is one?
Your insights are always helpful and appreciated.
Best Regards — Ahmed
MY REPLY:
Very interesting case — so much that I’d like to use it for an ECG Blog if you can give me follow-up.
I received 2 ECGs. The 1st one has the date of October 9 @ 7:23 on it — so it is a current (and not a previous tracing). But I have NO idea as to when this 1st ECG occurred with respect to the 2nd ECG that shows NSVT. Was the patient initially in sinus rhythm when she presented with “dizziness and palpitations” but no CP (chest pain)? Or was this after receiving Amiodarone. WHEN did she develop AFib?
ECG #2 shows as you say AFib with runs of NSVT (although since beats #1-thru-6 at the beginning of the tracing are all ventricular — we have no idea as to HOW LONG this first run was? (ie, it could have been sustained VT).
The few narrow (supraventricular) beats that we do see are irregularly irregular. So despite what looks like a “sinus P wave” in front of beat #23 in lead V3 — this is almost certainly a “fib wave” for a rhythm of underlying AFib.
The runs of WCT (wide-complex tachycardia) are fairly but not completely regular. There is a somewhat rightward frontal plane axis (more positive in II,III than in lead I) — and with lbbb-like conduction in the chest leads — BUT this is not “typical” lbbb conduction because there is already a predominantly positive QRS for the wide beats as early as lead V3 (and with true lbbb conduction, transition occurs later, typically by V5 or V6).
In addition — there is a “post-ectopic pause” after beats #6 and after #22 — and that is much more commonly seen following VT.
Finally — there is NO reason for aberrant conduction. Ashman occurs when you have a wide beat occurring after a relative pause ... See ECG Blog #70 and ECG Blog #71 for details about Ashman. But there is no preceding pause to set up conditions for aberrancy — and the same shape wide beat occurs for beats #10 and 14 despite different preceding coupling intervals. These are ventricular beats!
QRS morphology of these wide beats is consistent with RVOT VT (ie, lbbb-like in the chest leads; right frontal plane axis).
But GO BACK to ECG #1 — and note the flat (abnormal!) shape of the ST segment in lead V2 (should normally show a gently upsloping ST segment with slight ST elevation) and the clearly FLAT ST segments in V3,4,5 (and definite slight ST depression in V3). So if you only did a single normal Troponin — MORE troponin values should have been done since the 1st Troponin can sometimes be normal despite acute coronary occlusion.
Bottom Line — I am missing details as to what happened when ... but ECG #1 is not normal in a patient who develops runs of VT (and if this was the initial ECG before ECG #2, then I wonder if she had a silent acute posterior OMI?
ECG #2 shows AFib with runs of NSVT with RVOT VT morphology.
What happened? As I mentioned — I’d love to use this as an ECG Blog if you can answer some of my questions. I’d be happy to acknowledge you (a number of years ago I had you as from Amman, Jordan when you sent me a tracing that I published as a blog. Is that the way you would want me to acknowledge you? Or do you prefer for this case to be anonymous. Just let me know.
Hope the above is helpful —
ABBAS REPLY:
Dear Dr grauer
Thank you for your reply.
The ecg showing nsvt is the initial rhythm at presentation. Only complaining of dizziness, she came to the clinic at 16:45.
ECG with sinus rhythm was after we administered amiodarone and transported the patient, it was recorder at the receiving facility at 19:23.
I am not sure if they gave something else in the hospital, I will check tomorrow and let you know.
As for publishing, that would great but as anonymous, because I was not directly involved in the management of the patient,it is recorded in my new job in UAE,I am still new to the place and I don't want colleagues to accuse me of stealing there efforts.
Best regards — Ahmed Abbas
AHMED REPLY:
Dear Dr.Grauer, I hope you are well.
More update regarding the case:
the patient was admitted to the ccu under the diagnosis of paroxismal atrial fivrillation with intermittent preexcitation vs paroxysmal Afib with rate dependent abberancy.
they gave her 2 grams of magnesium ,stating in the order no BB/CCB or amiodarone.
after consulting EP the diagnosis changed to paroxismal afib with rate dependent abberat conduction vs frequent pvcs /RVOT ectopy.she was discharged on bisoprolol 5mg.
here echo was normal, they pointed that her troponin was elevated probably due to tachyarrhethmia/demand ischemia but i could not find the value of the troponin from her file or any new ECGs.
Best regards — Ahmed Abbas
MY REPLY (9/14/2026):
THANK YOU so much Ahmed for the additional information.
So if I understand you correctly — EP cardiology thought the diagnosis of the attached ECG was PAF ( = Paroxysmal AFib) with either: i) Rate-related aberrant conduction; — OR — RVOT runs of NSVT ( = non-sustained VT). Am I then correct that EP did not know for certain what the rhythm was?
Again — I feel runs of RVOT VT is more likely for the reasons that I stated …. at least based on the attached ECG.
- Do you know if the patient spent any time in the hospital? I’m asking because it seems like it would be risky to discharge the patient on low dose Bisoprolol unless they monitored the patient for a little time on this dose and saw that the arrhythmia was completely controlled. After all — we are considering runs of VT in the differential diagnosis?
THANKS! — : ) Ken
Good morning Dr. Grauer,
Yes. It seems from the files that she was monitored while on bisoprolol for 2 days in the ccu, then she was discharged on the same medication.
If there is anything significant in her EP follow-up appointment in few days I will inform you.
Best regards — Ahmed.
