ECG Blog #347 — Why Non-Conducted P Waves?

The lead III rhythm strip shown in Figure-1 — was obtained from an older woman following a syncopal episode. Her 12-lead ECG showed QRS widening in a nonspecific IVCD (IntraVentricular Conduction Defect) pattern — but did not suggest acute coronary occlusion. The patient was hemodynamically stable at the time the rhythm strip in Figure-1 was recorded.

CHALLENGE Questions:

Which one (or more) of the following choices is (are) correct?

• A normal sinus rhythm is present.
• There is AFib (Atrial Fibrillation). 
• AV dissociation is present.
• 3rd-Degree AV Block is present.
• Some type of Wenckebach conduction is present.

Figure-1: Long lead III rhythm strip — obtained from an older woman with syncope. How would YOU interpret the rhythm?

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• NOTE #1: As always — I favor the Ps, Qs & 3R Approach for interpretation of the cardiac rhythm (See ECG Blog #185). Assessment of these 5 parameters provides us with answers to the above Challenge Questions — and greatly narrows the possibilities for the rhythm diagnosis.
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• NOTE #2: Today’s tracing is slightly angled (slanted) — and as a result, measurements are slightly “off”. That said — this did not affect my overall interpretation of today's rhythm.

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Is AFib Present? — OR — Is there Sinus Rhythm?

P waves are definitely present in Figure-1 — which rules out the possibility of AFib. It’s clear that more than a single P wave is present within some of the R-R intervals — so a simple “sinus rhythm” is not present.

Is AV Dissociation Present?

AV dissociation is defined as the absence of any relationshipship between P waves and QRS complexes. This can be “complete” AV dissociation (in which case none of the P waves in the entire rhythm strip are related to any of the QRS complexes — as occurs with complete AV block) — or AV dissociation can be transient (that is, "intermittent" — or only occurring for one or more beats, but not for the entire tracing).

• Although at first glance it might seem as if there is AV dissociation in today's rhythm — a LOOK at Figure-2 reveals that this is not the case. WHY do I say this? 
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• HINT: What do the colored lines in Figure-2 suggest?

Figure-2: Why do the colored lines in this figure tells us that AV dissociation is not present?

Why AV Dissociation is Not Present:

Although the rhythm is not regular in Figure-2 — there is a pattern to this rhythm (ie, there is a "regular irregularity" to the rhythm). Thus, there is "group" beating (ie, alternating shorter-then-longer R-R intervals).

• Note that each of the shorter R-R intervals in Figure-2 (BLUE lines) — are of approximately equal length.
• Each of the longer R-R intervals (RED lines) — are also of similar (if not the same) length. This is not by chance!

PEARL #1: As emphasized in ECG Blog #186 — Whenever you see group beating in a rhythm — Consider the possibility of some type of Wenckebach conduction!

• The type of Wenckebach conduction that most providers are familiar with — is 2nd-degree AV Block of the Mobitz I Type — in which the PR interval progressively increases until a beat is dropped. Another name for Mobitz I = AV Wenckebach!
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• It's important to appreciate that there are many other examples of Wenckebach conduction! These include SA Wenckebach — AFib, AFlutter or ATach with Wenckebach conduction (in which there is group beating with Wenckebach periodicity) — junctional or ventricular rhythms with retrograde Wenckebach or with Wenckebach exit block — and many others.
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• PEARL #2: Although the specific mechanism for many of these types of Wenckebach conduction is complex (and beyond the scope of today's ECG Blog) — the "Take-Home" Point from today's post is to Consider some type of Wenckebach conduction whenever you see "group" beating. 
• Wenckebach conduction will not always be present in such cases (ie, you can see group beating with other rhythms — such as atrial bigeminy or trigeminy) — but prompt recognition of group beating when it does occur will facilitate rapid identification of Wenckebach rhythms! 

Continuing with Figure-2:

Did YOU Notice the repetitive pattern of PR intervals in Figure-2?

• Note that each of the shorter PR intervals in Figure-2 (YELLOW lines) — are of approximately equal length.
• Each of the longer PR intervals (GREEN lines) — are also of similar length. This is also not by chance!

BOTTOM Line for Figure-2:

AV dissociation is not present in Figure-2 — because all P waves are related in some way to neighboring QRS complexes. We know this — because the length of the 2 different PR intervals that we see in this rhythm (highlighted by the YELLOW and GREEN lines) are constantly repeated! This means that there must be some type of conduction!

• Since there is some type of conduction in Figure-2 — this rules out the possibility of 3rd-degree (complete) AV block! You can't have complete AV block IF there is some conduction.
• Instead — the fact that we see group beating in Figure-2 (in the form of alternating shorter-then-longer R-R intervals) — means that some form of Wenckebach conduction is probably present!

Is the Atrial Rhythm Regular?

Take another LOOK at today's rhythm (ie, See Figure-3).

• Is the atrial rhythm regular?

Figure-3: Take another LOOK at today's rhythm (which I've reproduced from Figure-1). Is the atrial rhythm regular? How can we tell?

PEARL #3: Wenckebach conduction is very commonly seen with both ATach (Atrial Tachycardia) and AFlutter (Atrial Flutter). Therefore — IF you see a fast and regular atrial rhythm in association with group beating — the underlying mechanism will usually involve some type of Wenckebach conduction.

• As I so often emphasize — Using calipers speeds up your interpretation and makes it EASY to determine if the underlying atrial rhythm is (or is not) regular.
• Find a place in the rhythm you are looking at where you can definitely see 2 P waves in a row (ie, Any of the longer R-R intervals in Figure-3 will do!). Set you calipers precisely to the distance between these 2 consecutive P waves — and it then becomes EASY to "walk out" P waves through the entire rhythm strip (ie, RED arrows in Figure-4).

PEARL #4: Once you've established that the atrial rhythm is regular — Determining the atrial rate provides an important clue to the type of atrial rhythm.

• As explained in ECG Blog #210 — the Every-Other-Beat Method for determining the ventricular rate — works equally well for determining the rate of fast atrial rhythms.

Figure 4: RED arrows highlight that the atrial rhythm in today's tracing is regular! Application of the Every-Other-Beat Method facilitates determining the rate of the atrial rhythm. Note that it takes just under 5 large boxes to record 2 P waves (YELLOW numbers in this Figure). Therefore — HALF the atrial rate is a little faster than 300/5 ~60-65/minute — which means that the actual atrial rate in today's tracing is ~2X this rate or ~125/minute. This is consistent with an atrial tachycardia (The atrial rate is not fast enough to be AFlutter). 

What We Do Know at This Point!

Although we have not yet determined the specific mechanism of today's rhythm — We have answered all 5 of the Challenge Questions:

• There is neither AFib nor simple sinus rhythm. The presence of regular P waves rules out AFib. The rapid atrial rate (ie, at ~125/minute) with failure to conduct all P waves rules out a simple sinus rhythm. Instead — there is atrial tachycardia.
• Group beating with 2 PR intervals that regularly repeat (as highlighted by the YELLOW and GREEN lines in Figure-2) — rules out 3rd-degree AV block and AV dissociation. Instead — these findings strongly suggest that some type of Wenckebach conduction is occurring.
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• PEARL #5: To Emphasize — the presence of Wenckebach conduction in association with either ATach or AFlutter does not necessarily indicate a pathological form of AV block! Instead — this may simply result from the rapid atrial rate (in which case it is possible that normal 1:1 AV conduction may resume once the rapid atrial rhythm resolves). Sometimes only clinical correlation and the passage of a little time will tell IF Wenckebach conduction that occurs in association with ATach or AFutter is (or is not) pathologic.
• That said — the patient in Today's Case is an older woman who presented with the rhythm in Figure-1 following a syncopal episode. In addition — QRS widening from a nonspecific IVCD was present on her 12-lead tracing. Therefore — any form of AV conduction disturbance has to be considered pathologic until proven otherwise!
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• KEY "Take-Home" Message from Today's Case: The specific mechanism for today's rhythm is complex. Full understanding by primary providers is not essential for appropriate management. Instead — it would be fine to stop your interpretation after establishing that today's rhythm shows atrial tachycardia with some form of Wenckebach conduction in this older patient with syncope who clearly needs further evaluation (and who may ultimately need a pacemaker). 

 

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Beyond-the-Core: The Specific Rhythm

Looking closer at Figure-4, in which we highlight regularly-occurring P waves throughout the entire tracing in today's rhythm — Aren't there P waves that we know are not being conducted to the ventricles?

• My answer to this question is proposed in Figure-5 — in which I highlight P waves that seem incapable of being conducted all the way to the ventricles (WHITE arrows in Figure-5).
• This leaves us with alternate R-R intervals in which we see 2 consecutive RED-arrow P waves. It's hard to imagine that both of these consecutive RED-arrow P waves (that occur between beats #2-3; 4-5; 6-7 and 8-9) — could be conducting to the ventricles. HOW then can we explain this?

Figure 5: WHITE-arrow P waves seem incapable of being conducted to the ventricles. But HOW to explain what is going on with alternate R-R intervals in which there are 2 consecutive RED-arrow P waves?

Dual-Level AV Block:

In ECG Blog #259 — I discussed the concept of Dual-Level AV Block (See the ADDENDUM below for an Audio Pearl review of this concept). In brief — Wenckebach conduction may occur at more than a single level as atrial impulses exit out of the AV Node. This concept is easiest to illustrate by means of a laddergram (See Figure-6).

• The atrial rhythm in the laddergram is illustrated by the regular vertical RED lines in the Atrial Tier.
• The horizontal BLACK dotted line schematically divides the AV Nodal Tier into 2 levels, each conducting impulses with its own degree of AV Block.
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• WHITE-arrow P waves do not make it through the upper AV Nodal level. Note that there is alternating 2:1 and 3:2 Wenckebach conduction in this upper AV Nodal level.
• PINK-arrow P waves make it through the upper AV Nodal level — but do not make it through the lower AV Nodal level.
• RED-arrow P waves make it through both AV Nodal levels — and are conducted to the ventricles. Note that there is 3:2 AV Wenckebach conduction through this lower AV Nodal level. 

Figure-6: My proposed laddergram for the mechanism of today's rhythm (See text).

CASE Conclusion:

The laddergram in Figure-6 makes sense — because all P waves and all QRS complexes in this tracing are accounted for. The underlying rhythm is atrial tachycardia with dual-level Wenckebach conduction out of the AV node, manifesting alternating 2:1 and 3:2 conduction at the upper AV Nodal level — and 3:2 AV conduction at the lower level.

• Clinically (as emphasized in the above Take-Home Message) — given the presentation of this patient with syncope, full evaluation of this older woman is indicated. Pending results — she may ultimately need permanent pacing (Unfortunately — I do not have specific follow-up on this case).
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• P.S.: For those wanting direction for how to derive a laddergram when there is dual-level AV Block — Please check out the Step-by-Step Laddergram illustration for a similar case in ECG Blog #259.

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Acknowledgment: My appreciation to Nizar Jiris (from Kfar Yasif, Israel) for allowing me to use this case and these tracings.

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Related ECG Blog Posts to Today’s Case: 

• ECG Blog #185 — Reviews the Ps, Qs & 3Rs Approach to systematic rhythm interpretation.
• ECG Blog #210 — Reviews the Every-Other-Beat Method for determining the rate of a fast regular rhythm.
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• ECG Blog #188 — Reviews the essentials for reading (and/or drawing) Laddergrams, with LINKS to numerous Laddergrams I’ve drawn and discussed in detail in other blog posts.
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• ECG Blog #186 — Highlights the importance of Group Beating — and reviews when to suspect the Mobitz I form of 2nd-Degree AV Block ( = AV Wenckebach).
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• ECG Blog #251 — Reviews the concepts of Wenckebach periodicity and the "Footprints" of Wenckebach (Please check out the Audio Pearl in this blog post that focuses on these concepts).
• ECG Blog #164 — Reviews a case of typical Mobitz I 2nd-Degree AV Block (with detailed discussion of the "Footprints" of Wenckebach). 
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• ECG Blog #259 — Reviews the concept of Dual-Level AV Block.
• The October 25, 2021 post in Dr. Smith's ECG Blog — My Comment (at the bottom of the page) reviews my approach to another case of a Dual-Level Wenckebach block. 
• ECG Blog #226 — Works through a complex Case Study (including an 11:00 minute ECG Video Pearl that walks you through step-by-step in the construction of a laddergram with Wenckebach conduction and dual-level block within the AV node).
• ECG Blog #243 — Reviews a case of AFlutter with Dual-Level Wenckebach out of the AV Node.

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ADDENDUM (11/28/2022): 

• For review on the concept of "Dual-Level" Wenckebach.

—  —

ECG Media PEARL #71 (5:45 minutes Audio) — Reviews the phenomenon of Dual-Level Wenckebach out of the AV Node (HOW to recognize this phenomenon — and how to distinguish it from Mobitz II).

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ADDENDUM (11/29/2021): I received a comment today on this tracing from David Richley, who is well known to most ECG enthusiasts who frequent any of the many ECG internet forums. Dave always offers the most astute commentary on complex Arrhythmia interpretation. NOTE: What follows below goes beyond-the-core! — But — It illustrates the important concept that complex arrhythmias may have more than a single potentially plausible interpretation.

• Dave writes the following: Hi Ken. I enjoyed your latest ECG blog (as always) — but while I agree that there is dual-level Wenckebach AV block — I could not explain why 2:1 block should alternate with 3:2 block in the upper AV node. What could be the physiological explanation for this? 
• I’ve come up with a modification of your hypothesis: I think there could be 5:4 Wenckebach AV block in the upper AV node — then 2:1 block of those impulses that reach the lower AV node, as illustrated in this laddergram. What do you think? — Dave —

Figure-7: Proposed laddergram submitted by David Richley.

MY Reply to Dave:

• Dave — I think both your laddergram and my laddergram are plausible. I always find it challenging with dual-level AV blocks — to try and figure out whether it is the upper or lower AV nodal level that has a higher degree of block. (Going back to some of the original articles on dual-level AV blocks — they describe even more than 2 levels of block within the AV node — so it can get even more complicated that what we see in today's rhythm).
• As per my Figure-6 — those beats with shorter PR intervals (ie, beats #1,3,5,7,9) — are preceded by longer R-R intervals — so I thought that might allow more time to recover, therefore allowing better (faster) conduction through the lower AV nodal level. I fully acknowledge that I may be wrong ...
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• BOTTOM LINE: The KEY point is in your initial sentence, in which you state how we both agree that there is dual-level AV block. The geometric relationships (with repeating PR and R-R intervals) are not by chance — do not represent complete AV block — but rather manifest some variation of AV Wenckebach conduction. On this we both agree! THANKS again for your always superb insights Dave!

 

ECG Blog #346 — Recurrent Palpitations

The ECG in Figure-1 — was obtained from a young woman with a history of recurrent palpitations over several years. She was hemodynamically stable at the time this tracing was recorded. ECGs, Echo and Holter monitoring on previous admissions had been normal.

• What is YOUR differential diagnosis of the rhythm? 
• What treatment is indicated?

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

MY Thoughts on the ECG in Figure-1:

The "good news" regarding today's case — is that this young adult woman with a history of presumably similar prior episodes — was hemodynamically stable at the time the ECG in Figure-1 was recorded.

• By definition — the fact that this patient was hemodynamically stable in association with the rhythm in Figure-1 means — that there was at least some time to contemplate the rhythm and formulate a plan for optimal management. Despite the fast rate in today's case — immediate cardioversion is not necessarily needed since the patient is stable!
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• To Emphasize: While true that many patients in sustained VT promptly deteriorate — others do not. I'm aware of many cases of sustained VT in which the patient remained awake, alert and hemodynamically stable for hours (and even days!). 
• BOTTOM Line: As long as you are right there at the bedside (ready to cardiovert at any moment should the patient deteriorate) — an initial trial of antiarrhythmic therapy is reasonable for a patient who remains hemodynamically stable despite sustained VT.

WHAT THEN is the Rhythm in Figure-1?

As always, once establishing that the patient in front of you is hemodynamically stable — I favor assessment of the rhythm by the Ps, Qs, 3R Approach (See ECG Blog #185):

• The rhythm in ECG #1 is fast and Regular. I estimate the Rate to be ~200/minute.
• I see no sign of atrial activity (ie, No P waves). 
• The QRS complex during the tachycardia is wide (I measure ≥0.12 second = 3 little boxes in duration).

IMPRESSION: The above parameters define the rhythm in Figure-1 as a regular WCT ( = Wide-Complex Tachycardia) at ~200/minute, without clear sign of atrial activity.

• As emphasized in many of my prior ECG Blogs (especially in ECG Blog #220) — the finding of a regular WCT rhythm without clear sign of atrial activity should always be assumed to be VT until proven otherwise (Statistical odds that a regular WCT rhythm without sinus P waves is VT — are ~80% in a previously healthy younger adult — and attain ~90% when the patient is older and has underlying heart disease).

PEARL #1: 80-to-90% is not 100%! Although we need to assume VT for any regular WCT rhythm without P waves until proven otherwise — sometimes the rhythm will be supraventricular!

• Assessment of QRS morphology helps greatly to narrow down the likelihood that a given WCT rhythm is either VT or an SVT (SupraVentricular Tachycardia) with preexisting BBB (Bundle Branch Block) or aberrant conduction (See ECG Blog #196 for details).
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• As emphasized in ECG Blog #211 — The chances of a WCT rhythm being supraventricular increase significantly IF — QRS morphology is consistent with one of the known forms of conduction block (ie, RBBB; LBBB; LAHB or LPHB; or RBBB with one of the hemiblocks).

Take another LOOK at the ECG in Figure-1:

• Does QRS morphology look like LBBB conduction?
• Is the rhythm in this tracing VT? — or — Is this SVT with LBBB conduction?

Figure-2: Take another LOOK at the ECG in today's case!

Is there Typical LBBB Morphology in ECG #1?

As emphasized in ECG Blog #204 — the 3 KEY leads for the ECG diagnosis of the bundle branch blocks are right-sided lead V1 — and left-sided leads I and V6.

• Assessment of these 3 KEY leads during the WCT rhythm in today's case is consistent with LBBB morphology — because we do see an all upright QRS in lateral leads I and V6 — and the QRS is predominantly negative in right-sided lead V1.

PEARL #2: The reason I favor focusing on leads I, V1, V6 — is that doing so allows rapid recognition of typical BBB morphology in a matter of seconds. However, when applying this concept to assessment of QRS morphology during a regular WCT rhythm — I look for a number of additional ECG findings that render QRS morphology during the WCT to be either more or less likely the result of VT.

• When assessing for LBBB Morphology: VT becomes more likely if one or more of the following atypical ECG findings are seen during the WCT: i) If the QRS complex is not all upright in both high-lateral leads (ie, not only in lead I — but also in lead aVL); ii) If the QRS complex is not predominantly negative in at least the first 4 chest leads (ie, not only in V1,V2 — but also in V3,V4); and, iii) If there are unexpected Q waves in lateral and/or in anterior leads — especially if these initial unexpected Q waves are wide.
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• When assessing for RBBB Morphology: SVT becomes more likely if QRS morphology is completely typical for this conduction defect — which means: i) There is a completely typical rsR' complex in lead V1 (ie, with an s wave that descends below the baseline — and a taller right "rabbit ear" R' wave); and, ii) There are upright R waves with wide terminal S waves in lateral leads I and V6.

We have previously shown cases for the diagnostic dilemma that arises when QRS morphology of a WCT resembles RBBB conduction (See ECG Blog #323 — ECG Blog #38 — and ECG Blog #85). In contrast — today's case highlights the dilemma when QRS morphology for a regular WCT resembles LBBB conduction.

• To Emphasize: None of the "rules" for assessing QRS morphology during regular WCT rhythm are perfect. Exceptions always exist. For example — QRS morphology may be dramatically altered in a "baseline" ECG in patients who have significant underlying heart disease. In such cases — QRS morphology will not resemble a "typical" conduction defect when heart rate increases.

• PEARL #3: When possible — Try to find a prior ECG on the patient! Doing so will occasionally allow you to make a definitive diagnosis of a supraventricular rhythm IF — QRS morphology on the baseline ECG is identical to QRS morphology during the WCT. Then after successful treatment — Be sure to obtain a post-conversion 12-lead ECG for comparison purposes.

Returning to Today's CASE:

Although the ECG in Figure-2 superficially resembles LBBB conduction — there are some atypical features. As noted above in PEARL #2:

• Although the QRS complex in lead V6 is perfectly consistent with LBBB conduction (because the QRS is tall and all upright in this lead) — the QRS in lead I is of much smaller amplitude (and the QRS is barely positive in several of the complexes in lead I). In lead aVL — the QRS is all negative! Therefore — QRS morphology in leads I and aVL is not typical for LBBB conduction.
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• In the chest leads — the QRS is predominantly negative (as it should be with LBBB conduction) in leads V1 and V2. However, the QRS abruptly becomes all positive beginning in lead V3 — which is clearly much earlier that expected with LBBB conduction!
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• Putting It All Together: As emphasized above — Statistical odds that a regular WCT rhythm without clear sign of sinus P waves will turn out to be VT are ~80-90% even before you look at the ECG. Thus, we begin from the premise that the regular WCT in today's case should be assumed  VT until proven otherwise. Add to this the 2 atypical features for LBBB conduction described above — and statistical odds that the rhythm in Figure-2 is VT are over 90%!
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• PEARL #4: In view of the fact that the patient in today's case is a younger adult without underlying heart disease (ie, normal Echo on prior admissions) — the rhythm most probably is Idiopathic VT. As summarized in the ADDENDUM below — approximately 10% of patients who present with VT do not have ischemic or underlying structural heart disease. Short- and longterm treatment (as well as prognosis) of such patients differs greatly compared to that for the ~90% of patients with ischemic or structural forms of VT.
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• As discussed in Figure-3 — QRS morphology for the VT rhythm in today's case manifests a LBBB pattern in the chest leads (ie, with predominant negativity in V1,V2 — and a completely positive QRS in lateral chest leads) — but with a vertical (inferior) axis in the frontal plane (ie, marked QRS positivity in the inferior leads compared to lead I). This suggests the OT (Outflow Track) form of VT. Early transition to an all positive QRS already by lead V3 in the chest leads suggests LVOT (Left Ventricular Outflow Track) VT. 
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• With Respect to Treatment: Regardless of whether today's rhythm is RVOT VT or LVOT VT — both of these forms of idiopathic VT tend to be "Adenosine-responsive". Adenosine would therefore be my initial drug of choice for treatment of today's patient in the ED.

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Acknowledgment: My appreciation to Mubarak Al-Hatemi (from Qatar) for the case and this tracing.

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ADDENDUM (11/23/2022):

• KEY features of Idiopathic VT are summarized in Figure-3.

Figure-3: 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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Additional Relevant ECG Blog Posts to Today’s Case:

• ECG Blog #185 — Reviews my System for Rhythm Interpretation, using the Ps, Qs & 3R Approach.
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• ECG Blog #210 — Reviews the Every-Other-Beat (or Every-Third-Beat) Method for estimation of fast heart rates — and discusses another case of a regular WCT rhythm.
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• ECG Blog #220 — Review of the approach to the Regular WCT (Wide-Complex Tachycardia).
• ECG Blog #196 — Reviews another Case with a Regular WCT Rhythm. 
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• ECG Blog #204 — Reviews the ECG diagnosis of the Bundle Branch Blocks (RBBB/LBBB/IVCD). 
• ECG Blog #203 — Reviews ECG diagnosis of Axis and the Hemiblocks. For review of QRS morphology with the Bifascicular Blocks (RBBB/LAHB; RBBB/LPHB) — See the Video Pearl in this blog post.
• ECG Blog #211 — WHY does Aberrant Conduction occur?
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• ECG Blog #197 — Review of Fascicular VT.
• ECG Blog #301 — Reviews a WCT that is SupraVentricular! (with LOTS on Aberrant Conduction).
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• ECG Blog #323 — Review of Fascicular VT.
• ECG Blog #38 and Blog #85 — Review of Fascicular VT.
• ECG Blog #278 — Another case of a regular WCT rhythm in a younger adult.
• ECG Blog #35 — Review of RVOT VT.
• ECG Blog #42 — Comprehensive review of criteria for distinguishing VT vs Aberration.

ECG Blog #345 — Forward - Backward Conduction?

The ECG in Figure-1 — was obtained from a previously healthy young man who presented with “rapid heart beat”. He was hemodynamically stable at the time this ECG was recorded.

• How would YOU interpret this ECG?
• Is there any atrial activity?
• Are AFlutter (Atrial Flutter) and Sinus Tachycardia in your differential diagnosis?

Figure-1: The initial ECG in today’s case — obtained from a previously healthy young adult who presented with “rapid heart beat” (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the ECG in Figure-1:

As always — I favor beginning my interpretation of a 12-lead ECG with assessment of the cardiac rhythm — before addressing the 12-lead ECG. As per ECG Blog #185 — I favor the Ps, Qs, 3R Approach, beginning with whichever of these 5 parameters is easiest to assess for the tracing in front of me:

• The rhythm in Figure-1 is fast and Regular.
• The QRS is narrow in all 12 leads (ie, The QRS is not more than half a large box in duration = not more than 0.10 second). Therefore — the rhythm is supraventricular!
• Normal sinus P waves are absent (ie, there is no regularly-occurring, upright P wave in lead II).
• The Rate of the rhythm is ~190/minute. 

PEARL #1: In my experience — the easiest way to accurately estimate heart rate when the rhythm is rapid and regular — is by the Every-Other-Beat Method (See ECG Blog #210). The reason this is clinically relevant in today’s case — is that accurate estimation of the heart rate significantly narrows our differential diagnosis for determining the cardiac rhythm.

• To apply the method — Find a part of a QRS complex in any of the 12-leads, that begins or ends on a heavy ECG grid line. In Figure-2 — the peak of the R wave in lead III begins just after the 1st vertical RED line.
• As shown by the RED numbers — the R wave of the 3rd QRS complex in lead III (ie, the R-R interval of every-other-beat) occurs just over 3 large boxes later.
• Therefore — the amount of time needed to record 2 beats (BLUE numbers in Figure-2) — is just over 3 large boxes. This means that HALF the rate is a little bit less than 300 ÷ 3 or ~95/minute. The actual heart rate is TWICE this amount (ie, ~95 X 2  = 190/minute). 

Figure-2: Use of the Every-Other-Beat Method — for rapid estimation of heart rate (See text).

PEARL #2: From the parameters that we’ve just assessed — the rhythm in Figure-2 is a Regular SVT (SupraVentricular Tachycardia) at a rate of ~190/minute, but without clear sign of sinus P waves (ie, without a definite upright P wave in lead II). This description should prompt consideration of the followling differential diagnosis:

• i) Sinus Tachycardia (IF there is a possibility that sinus P waves might be hiding within the preceding ST-T wave); 
• ii) A Reentry SVT (either AVNRT if the reentry circuit is contained within the AV node — or AVRT if an AP [Accessory Pathway] located outside the AV node is involved); 
• iii) Atrial Tachycardia (ATach);
• iv) Atrial Flutter (AFlutter) with 2:1 AV conduction.

KEY Point: Although other entities may also produce a regular SVT (ie, sinoatrial node reentry tachycardia, junctional tachycardia) — they are far less common in practice. Therefore, remembering to think of the 4 entities in the above LIST whenever you encounter a regular SVT rhythm without clear sign of sinus P waves — will greatly facilitate determining the correct diagnosis.

PEARL #3: How Heart Rate Helps in SVT Diagnosis:

• Sinus Tachycardia usually does not exceed 160-170/minute in a "horizontal" adult (ie, in a patient you are examining, who has not just been running or performing another form of active exercise). This is not to say that sinus tachycardia will never go faster than 170/minute — but rather to suggest that when the rate of the regular SVT rhythm you are assessing is clearly over this rate range — then the rhythm will usually not be sinus tachycardia. 
• NOTE: All bets are off in children — in whom sinus tachycardia at a rate over 200/minute is not that uncommon.
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• With AFlutter — the most common ventricular response in the patient who is not being treated with an antiarrhythmic medication 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. As a result — IF the ventricular rate of the regular SVT rhythm you are assessing is over ~170-180/minute — then AFlutter is much less likely, because this rate would be faster-than-expected for 2:1 AV conduction, and too slow for 1:1 AV conduction. 
• KEY Point: This ~140-160/minute rate range is for untreated AFlutter. Patients who are already on antiarrhythmic medication may present with a slower atrial rate (and therefore a slower ventricular response) for AFlutter.
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• NOTE: Keep in mind that ATach is less common as a cause for a strictly regular SVT, especially in an otherwise healthy young-to-middle-aged adult. ATach is more likely to be seen in patients referred for EP (ElectroPhysiologic testing) — and in older adults with SSS (Sick Sinus Syndrome). As noted in PEARL #2 — I include ATach in the above Regular SVT differential diagnosis LIST for completeness — but in a non-EP-referral practice, ATach will not be seen nearly as often as AFlutter and the reentry SVTs.
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• SUMMARY: IF the rate of a regular SVT without clear sign of sinus P waves is substantially faster than 160-170/minute — then a reentry SVT rhythm (ie, AVNRT or AVRT) becomes the most likely diagnosis. However, IF the rate of the regular SVT is close to 150/minute (ie, 140-160/minute) — then any of the 4 diagnostic entities in the above LIST from PEARL #2 could be present ( = Sinus Tach — AVNRT-AVRT — ATach — AFlutter).

Regarding Today's CASE:

As derived above — today's case features a completely regular SVT rhythm without sinus P waves — at a rate of ~190/minute. 

• Given this rapid a rate — Sinus tachycardia and AFlutter are both unlikely (See PEARL #3). 
• Statistically — the completely regular SVT rhythm that is seen in Figure-2 will less often be the result of ATach. 
• This leaves a reentry SVT (ie, AVNRT or AVRT) — as the most likely diagnosis.
• 
  
• The "Good News" — is that regardless of whether the rhythm in today's case is AVNRT or AVRT — both rhythms usually respond to either Adenosine or use of some other AV nodal blocking agent (ie, Verapamil, Diltiazem, a ß-blocker).

QUESTION:

• Although sinus P waves are absent in ECG #1 — Could there be other evidence of atrial activity?
• 
  
• HINT: What might the RED arrows in Figure-3 be pointing to?

Figure-3: What might the RED arrows be pointing to?

What Might the RED Arrows Be?

Subtle signs of atrial activity during a regular SVT rhythm may provide an important clue to the etiology of the arrhythmia.

• Retrograde atrial activity during an SVT rhythm is most easily recognized by the finding of negative P waves in one or more of the inferior leads. This negative P wave deflection may be seen as a notch in the terminal portion of the QRS complex — as a notch in the ST-T wave — or sometimes beyond the end of the T wave.
• Other leads that I have found most helpful for recognizing retrograde atrial activity are lead aVR and lead V1. When seen in these leads — retrograde atrial activity appears as a positive deflection.
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• KEY Point: The distance from the onset of the R wave until the beginning of the retrograde P wave is known as the RP' interval.
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• IF retrograde P waves are seen in a regular SVT rhythm — and the RP' interval is short (ie, ≤70 msec.) — then AVNRT (AtrioVentricular Nodal Reentrant Tachycardia) in which the reentry circuit is entirely contained within the AV node becomes more likely! (González-Torrecilla et al: Ann Noninvasive Electrocardiol 16(1):85-95, 2011).
• In contrast, when the RP' interval is somewhat longer — then AVRT (AtrioVentricular Reciprocating Tachycardia) in which the reentry circuit involves both the AV node and passage outside of the AV node to involve an AP (Accessory Pathway) becomes more likely.
• Because precise measurement of the RP' interval is often difficult — I consider the RP' interval to be short (ie, predictive of AVNRT) if retrograde P waves either notch the end of the QRS, or occur very soon after the QRS (See ECG Blog #240 for detailed discussion of these RP' concepts).
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• Regarding Today's Case: While difficult to be certain — I suspected that the deepest part of the negative T waves in the inferior leads and the peak of the T waves in leads aVR and V1 were more pointed than expected (RED arrows in Figure-3). IF these peaked deflections did indeed represent retrograde atrial activity — then the RP' interval would be relatively long. This would support the likelihood of orthodromic AVRT (ie, with the impulse initially traveling down the normal AV nodal pathway to enter the ventricles — followed by retrograde passage of the reentry circuit returning to the atria via conduction over an AP).
• 
  
• To Emphasize — Whether or not an AP was participating in the reentry circuit of the SVT rhythm in today's case should not affect clinical decision-making. This is because AV nodal blocking agents should work regardless of the mechanism of this reentry SVT rhythm.

Conclusion of Today's CASE:

The patient in today's case was treated with IV Adenosine. The result of this treatment is shown in Figure-4.

• What happened?

Figure-4: The repeat ECG after administration of IV Adenosine. (To improve visualization — I've digitized the original ECG using PMcardio).

The Result of Treatment:

Treatment with IV Adenosine resulted in prompt conversion to sinus rhythm (Figure-4). Although fairly normal sinus P waves are now seen in lead II — the PR interval is clearly shortened in each of the chest leads. The QRS complex is wide — and a distinct delta wave is seen in each of these chest leads (BLUE arrows).

• This post-conversion tracing in Figure-4 reveals that today's patient has WPW (Wolff-Parkinson-White) Syndrome. Because delta waves were not seen during the tachycardia — this patient's AP was "concealed" during the SVT rhythm.
• In retrospect — the RED arrows I highlighted in Figure-3 did in fact represent the result of retrograde atrial activity returning to the atria over the AP (thereby producing the relatively long RP' interval).
• 
  
• Final POINT: The patient in today's case may not necessarily need ablation of the AP. Whether or not this patient should be referred to EP Cardiology should depend on: i) What the patient wants to do! — and — ii) How often his SVT episodes occur — how long episodes last — and how difficult it is (or is not) to control episodes by attention to potential precipitating factors and/or with medication (See ECG Blog #155 for discussion of the management of newly discovered WPW).

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Acknowledgment: My appreciation to an anonymous sender (from Malaysia) for the case and this tracing.

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ADDENDUM (11/18/2022):

• I have previously presented the material in the 2 Audio Pearls below — but this content bears repeating for easy reference. Appreciation of these concepts should be automatic for assessment of the patient who presents with a regular SVT rhythm.

—  — 

Today's ECG Media PEARL #55 (4:20 minutes Audio) — What does the term, "SVT" mean? This Audio Pearl reviews the semantics and clinical application involved in use of this term. 

—  —

Today's ECG Media PEARL #64 (10:50 minutes Audio) — Reviews my LIST #2: Common Causes of a Regular SVT Rhythm.

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Additional Relevant Material to Today's Case:

• See ECG Blog #185 — for review of the Systematic Ps, Qs, 3R Approach to rhythm interpretation.
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• See ECG Blog #240 — for Review on the ECG assessment of the patient with a regular SVT rhythm (including distinction between the various types of SVT reentry).
• See ECG Blog #250 — for Review of another case of a regular SVT with ST depression.
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• ECG Blog #210 — reviews the Every-Other-Beat Method for rapid estimation of heart rate.
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• ECG Blog #220 — reviews my LIST #1: Causes of a Regular WCT and — HOW to assess Hemodynamic Stability (Listen to Audio Pearl #37 in this post).
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• ECG Blog #229 — reviews distinction between AFlutter vs ATach (and WHY AFlutter is so commonly overlooked). 
• The November 12, 2019 post in Dr. Smith's ECG Blog — in which I review my approach to a Regular SVT rhythm.
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• González-Torrecilla et al: Ann Noninvasive Electrocardiol 16(1):85-95, 2011 — Reviews distinction between AVNRT vs AVRT and other regular SVT rhythms in patients without WPW.