What could this rhythm be? And what is going on after it breaks?

Written by Pendell Meyers, edits by Steve Smith


A man in his 30s with no prior medical history presented with palpitations. His vitals and exam were within normal limits with the exception of his heart rate.

Here is his initial ECG:

What do you think? What is the differential?

This shows a regular narrow complex tachycardia, thus the differential is sinus tach, SVT (including AVNRT most commonly, AVRT [which is SVT in the setting of WPW with an accessory pathway] next most common, then atrial tachycardia, etc.) or atrial flutter.

It it were atrial flutter, and because it is regular at a rate of 210, the flutter would have to be conducting 1:1 to the ventricle. There are no definite atrial waves, although the negative deflections in V1 before the QRS complexes could be atrial in origin, or the entire baseline may appear to have a sawtooth pattern in lead II - it is not clear in my opinion. 1:1 atrial flutter seems unlikely because, as it would have to be 1:1 conduction, the atrial flutter rate would have to be a very slow 210 bpm (normal would be 300). The ventricular rate of roughly 210 bpm makes sinus tachycardia unlikely in a 30 year old (max sinus rate theoretically 190ish according to 220-Age rule of thumb).

Aside: if the atrial flutter rate were 300 bpm, it could not be conducted by the AV node, and the ventricular rate could only be 300 if there were an accessory pathway or a peri-AV node bypass tract that inserts into the bundle of His. In the former case, there would have to be a wide QRS (due to the preexcitation of the delta wave), but in the latter case, the QRS would be narrow.



The REVERT vagal maneuver was performed with a change in rhythm.


A repeat ECG was performed:

What do you think?

There is now a regular rhythm with wider QRS complexes than during the tachycardia above, almost imitating LBBB. There is an extremely short PR interval, such that the wide QRS takes off from the end of the P-wave. The takeoff of the QRS complex is not the most obvious delta wave, but overall this appears consistent with accessory pathway conduction, or WPW.

See these two similar cases:

A 40-something woman with no medical history presented with 2 days of chest pain

What do you think about this Left Bundle Branch Block?

Now that we suspect the patient has an accessory pathway, the most likely rhythm responsible for his paroxysmal narrow complex regular tachycardia in the first ECG is orthodromic AVRT, in which the action potential is conducted down the AV node (causing a narrow QRS complex) and then up the bypass tract, and so on.


The patient was referred to EP for an EP study and possible ablation.


Learning Points:

You must easily be able to think through the differential of tachycardias based on the categories of narrow vs. wide QRS and regular vs. irregular rhythm:
 - Narrow & Regular
 - Narrow & Irregular
 - Wide & Regular
 - Wide & Irregular

After conversion from a regular, narrow complex tachycardia, you should always obtain a post-cardioversion ECG to look for the presence of underlying causes of the tachycardia, most commonly WPW syndrome.

WPW can distort the QRS complex and mimic bundle branch blocks or other conduction abnormalities, without showing the classic delta wave into an otherwise normal, narrow QRS complex. The risk in this case is that WPW is missed due to the confusing QRS morphology.

Some bypass tracts are "concealed" meaning they do not conduct during normal sinus rhythm and thus leave no evidence on the resting sinus ECG.

===================================

MY Comment by KEN GRAUER, MD (10/16/2019):

===================================

Excellent case for discussion presented by Drs. Meyers & Smith! I would add the following comments regarding selected concepts of arrhythmia diagnosis and management:

Use a Systematic Approach: There are 6 KEY parameters to assess when confronted with any cardiac arrhythmia. These 6 parameters are:

• #1) Is the patient hemodynamically stable? This clearly is the 1st thing to assess — since if the patient is not hemodynamically stable because of the arrhythmia — then immediate cardioversion is indicated regardless of whether one is dealing with VT or an SVT.

The Next 5 Parameters constitute what needs to be assessed regarding the arrhythmia itself. I find it easiest to remember these parameters by the saying, “Watch your Ps, Qs and the 3 Rs”:

• Are there P waves? And, if there aren’t clearly identifiable P waves — Is there evidence of atrial activity, such as “fib” or “flutter” waves?
• Is the QRS complex wide or narrow?
• What is the Rate?
• Is the rhythm Regular?
• If P waves are present — Are they “Related” to neighboring QRS complexes?
• CLICK HERE — if interested in more on using the “Ps, Qs & 3Rs” Approach.

Figure-1: The 2 ECGs in this case (See text).

Assessing the 6 Parameters in This Case:

For clarity — I’ve put the 2 tracings in this case together in Figure-1. Although there is some angulation of these tracings — measurements are intact.

• Regarding the 6 Parameters: The patient in this case was symptomatic with “palpitations” — but this man in his 30s was hemodynamically stable with normal vital signs other than a fast heart rate.
• Normal sinus P waves (ie, upright P waves in lead II) are not seen. There may be 1:1 retrograde activity (RED arrows in ECG #1) — but if these sharper-than-expected deflections do reflect retrograde atrial activity — the RP’ interval would be relatively long (occurring well within the ST segment). RP’ intervals occurring well within the ST segment are too long to be consistent with AVNRT — but could be consistent with orthodromic AVRT (since it takes more time for retrograde conduction over an accessory pathway that lies further away, because it is outside of the AV node).
• The QRS complex is narrow (ie, clearly not more than half a large box in duration in any of the 12 leads in ECG #1).
• The 3 Rs: The ventricular rhythm is extremely Regular — the Rate is ~210/minute — and although no sinus P waves are present, P waves could be “Related” to neighboring QRS complexes by 1:1 retrograde = VA conduction.

CONCLUSION: The patient is hemodynamically stable. The rhythm in ECG #1 is a regular SVT (SupraVentricular Tachycardia) at ~210/minute without clear sign of sinus P waves. As mentioned, there may be 1:1 retrograde atrial conduction — but it is difficult to be certain about this from ECG #1. As per Dr. Meyers — the principal differential diagnosis of a regular SVT without clear sign of sinus P waves includes: i) Sinus Tachycardia; ii) Reentry SVT (either AVNRT if the reentry circuit is contained within the normal AV nodal pathway — or AVRT if an accessory pathway is involved); iii) Atrial Tachycardia; or iv) Atrial Flutter.

NOTE: It is worth spending a moment on how we determined the heart Rate — since accurate estimation of rate can sometimes be extremely helpful in determining which of the above diagnostic considerations is the most likely cause of a regular SVT rhythm.

• When the rhythm is fast and regular — the Every-Other-Beat Method allows rapid and accurate rate estimation. Find a QRS complex that begins on a heavy line. We chose the 2nd beat in lead I (See the 1st vertical RED line under this beat in lead I of ECG #1).
• The amount of time (ie, the R-R interval) that it takes to record 2 beats (BLUE numbers in lead II) is just under 3 large boxes (RED numbers in lead I). Therefore — HALF the rate is a little faster than 300/3 ~105/minute.
• The actual rate for the rhythm in ECG #1 is therefore ~105 X 2 = 210/minute.
• CLICK HERE — if interested in brief video review of this Every-Other-Beat Method.

How Heart Rate Helps in SVT Diagnosis:

• Although the formula for estimating the maximal rate of sinus tachycardia for stress testing (ie, during exercise) is ~ 220 minus Age — in my experience, it is highly unlikely (though not impossible) for sinus tachycardia in a “horizontal" adult patient (ie, in a patient you are examining, who has not just been running) to exceed 170/minute. This statement does not hold true for children — as sinus tachycardias over 200/minute are not that uncommon in the pediatric age group. But the rate of 210/minute for the patient in this case essentially rules out sinus tachycardia.
• The most common ventricular response to untreated AFlutter is ~150/minute (usual range ~140-160/minute). This is because the atrial rate in untreated AFlutter is most often ~300/minute (usual range 250-350/minute) — and since untreated AFlutter most often presents with 2:1 AV conduction — 300/2 ~150/minute. Therefore (as per Dr. Meyers) — the SVT in this case at a rate of ~210/minute is highly unlikely to be AFlutter in this previously healthy man in his 30s, since this would entail a flutter rate of 210 X 2 = 420/minute, which is much faster the atrial rate for flutter. NOTE: This rate range is for untreated AFlutter. Patients who are already on antiarrhythmic medication may present with a slower atrial (and therefore ventricular) rate for flutter.
• Finally — Although listed in the above differential diagnosis — ATach is far less common as a cause for a strictly regular SVT as seen in ECG #1 compared to AVNRT or AVRT, especially in a previously healthy younger adult.
• THEREFORE — By the process of elimination, the most likely cause of the regular SVT at ~210/minute in ECG #1 is a reentry tachycardia. And, if the RED arrows we’ve drawn in ECG #1 do in fact represent retrograde atrial activity with a long RP' interval — then it’s likely this patient has WPW (CLICK HERE — for review of the common arrhythmias encountered with WPW).
• PEARL: From the above, it can be seen that if the regular SVT is at a rate close to 150/minute (ie, 140-160/minute) — that any of the 4 diagnostic entities listed above could be present (sinus tach/AVNRT-AVRT/ATach/AFlutter). It is when the rate of a regular SVT without clear sign of sinus P waves is substantially faster than this — that a reentry SVT (AVNRT/AVRT) becomes by far the most likely diagnosis!

FOLLOW-UP: As per Dr. Meyers — ECG #2 was obtained after the vagal maneuver. I’ve drawn BLUE arrows to highlight those leads in which delta waves are seen — which confirms the diagnosis of WPW.

Should This Patient be Ablated?

The patient in this case was a previously healthy man in his 30s, who presented with “palpitations”. There is no mention of prior episodes of SVT. There is no mention of drug therapy — only that the REVERT vagal maneuver was performed and was successful. Is EP referral for ablation the optimal course of treatment for this patient? In my opinion — the answer is not a yes — but rather, “It depends” ...

• Clearly the approach to treatment of numerous cardiac arrhythmias has changed in recent years, with ever increasing expertise in the exciting field of cardiac electrophysiology. But even in the best of centers with the most experienced of EP cardiologists — ablation IS a procedure, and there IS potential for adverse effect.
• If I was a previously healthy 30-year old man with a 1st episode of a hemodynamically tolerated SVT that was easily resolved by simple vagal maneuver (without even need for antiarrhythmic medication) — I would not opt for an invasive procedure with potential for significant side effects as my 1st intervention (despite VERY high likelihood for “cure” of this arrhythmia with very low chance of adverse effect). “Low risk” is not the same as “NO risk” — and if I was the patient, I'd prefer to start with a far less invasive intervention.
• That said — there is not a Yes-or-No answer to this question. I’m simply suggesting that rather than automatically referring this patient to EP cardiology for ablation of his accessory pathway at this point — that an appropriate alternative course might be diligent follow-up while teaching this patient vagal maneuvers that he can perform at home on his own (ie, Valsalva), perhaps with a prn antiarrhythmic “cocktail” (ie, a single dose of beta-blocker or diltiazem or verapamil) that can be tried if this hemodynamically stable SVT recurs. Recurrence of this SVT might be infrequent (if it recurs at all), and it might again be easily managed — possibly even without need for daily antiarrhythmic therapy.
• NOTE: ED referral of this patient for follow-up care IS of course indicated! — but such follow-up need not necessarily be to an EP cardiologist (or even necessarily to a cardiologist). Of course — IF repeated episodes occurred despite appropriate antiarrhythmic medication — that would be a different story (in which case, referral to your friendly EP cardiologist becomes the optimal management approach). Along the way to guiding optimal decision-making for this case — informed patient consent and patient preference are critical.
• CLICK HERE — for more on “My Take” on How to Advise the Patient with WPW.

Our THANKS to Drs. Meyers and Smith for presenting this case!