ECG Blog #539 — Does SVT cause Hypotension?

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).

Review of some Clinical Concepts:

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 the QRS clearly measures ≥0.11 second in duration. And the easy way to tell if QRS duration is ≥0.11 second — is to determine if QRS duration is clearlly more than 1/2 a large box in duration (ie, Each large box on ECG grid paper = 0.20 second ==> 1/2 a large box = 0.10 second, and if the QRS is more than this — then by my definition it is wide!).
• PEARL #2: Just because a given diagnosis is written in a patient's chart — does not necessarily mean that diagnosis is correct (unless you also find firm objective evidence in that patient's chart to support the diagnosis!). We need to remain open to other possibilities. Therefore, in today's case — I did not fully accept the prior "history of recurrent SVT" — because I was not shown any prior ECG documenting that the known tachycardia was indeed supraventricular.
• 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 — 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 is clearly 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). For example:

• We've seen a number of patients in sustained VT remain hemodynamically stable not only for hours — but for days!
• In contrast, most otherwise healthy younger adults who present in a sustained SVT rhythm — will remain stable for long periods of time.
• Bottom Line: The fact that today's patient was hypotensive in association with the rhythm in Figure-1 is not reliably predictive of this rhythm's etiology. That said — it is indication of the need for prompt effective therapy (ie, having a lower threshold to proceed with synchronized cardioversion).

The ECG in Figure-1:

As already noted — the rhythm in Figure-1 is a regular WCT at a rate of ~180-190/minute. With regard to atrial activity — there is no consistent sign of upright sinus P waves in lead II, or in any other lead. That said — the negative notching in the terminal portion of the QRS in leads II and aVF suggests there are 1:1 retrograde P waves (YELLOW arrows in Figure-2).

• PEARL #5: Even if the negative notching highlighted by YELLOW arrows in Figure-2 does represent 1:1 retrograde P waves — this does not help in our differentiation of the rhythm because both VT and reentry SVT rhythms may manifest 1:1 VA conduction.

Figure-2: YELLOW arrows highlight what appears to be 1:1 retrograde P waves.

What about QRS Morphology?

Up until this point — We've highlighted this young woman's history, namely of recurrent SVT, with today's episode thought to represent just one more recurrence. That said, because the QRS in Figure-1 is wide — We need to consider the possibility of VT.

• PEARL #6: 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 #7: As discussed below in the ADDENDUM to today's post — 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/hemiblock conduction!

NOTE: As shown in Figure-3 — QRS morphology is not typical for RBBB with either left anterior or posterior hemiblock.

• Instead of the expected triphasic rsR' complex in lead V1 (with taller right "rabbit ear" and a distinct S wave that descends below the baseline) — a qR pattern is seen in this lead. While SVT rhythms do not always show "typical" QRS morphology — it's important to appreciate that atypical conduction features may be a hint of a ventricular etiology (See Figure-9 in the ADDENDUM below).
• Typical RBBB conduction should manifest a wide terminal S wave in left-sided leads I and V6. While we do see a wide terminal S wave in lead I — this feature is missing in lead V6 (ie, the deep S wave in lead V6 in Figure-3 is narrow and followed by a small positive deflection = an RSr' in lead V6).
• With RBBB conduction — left-sided lead I typically manifests predominant positivity prior to the wide terminal S wave. However, the R wave in lead I in Figure-3 is relatively small.
• QRS morphology in leads II and III is not typical for either LAHB or LPHB conduction (ie, leads II and III lack the predominant positivity of LPHB — and the rSr' pattern in lead III is not the expected rS pattern typical of LAHB conduction).

BOTTOM Line: While the above subtle morphologic features do not rule out the possibility of an SVT rhythm for today's tracing — they should increase our suspicion that the rhythm in Figure-3 may represent fascicular VT.

• PEARL #8: Assessment of QRS morphology on the surface ECG is not definitive for distinguishing between SVT vs VT. Sometimes the only way to determine the true etiology of a regular WCT rhythm is by EP testing. That said — especially given the history in today's case of recurrent episodes — these atypical morphologic features made me highly suspicious that the rhythm in Figure-3 was probably fascicular VT.

PEARL #9: As has been emphasized on many posts in this ECG Blog — the treatment of choice for a hemodynamically stable patient in fascicular VT is IV Verapamil (or IV Diltiazem).

• Although Adenosine may convert some cases of fascicular VT — it is much less effective than IV Verapamil in this group of patients.
• IV Verapamil or IV Diltiazem should not be given to patients with ischemic VT (ie, in patients with underlying structural heart disease). This is because the negatively inotropic and vasodilating effects of these drugs may lead to hemodynamic decompensation. However, these drugs are safe in patients with idiopathic VT who do not have underlying heart disease.
• The extra advantage of using IV Verapamil to treat an otherwise healthy younger adult with suspected fascicular VT — is that this drug is likely to be effective regardless of whether the rhythm is fascicular VT or a reentry SVT rhythm!
• The above said, since today's patient was hypotensive in association with the rhythm in Figure-1 — the treatment of choice is synchronized cardioversion.

Figure-3: QRS morphology in today's tracing is not typical for RBBB/hemiblock conduction.

One More Clue to Today's Rhythm!

Take another LOOK at today's rhythm in Figure-4.

• Could the slanted RED lines in Figure-4 represent atrial activity?

Figure-4: What do the slanted RED lines indicate?

Answer:

Overall — there is very little artifact in Figure-4. As a result — I was struck by the consistent disturbance in the baseline in lead II that has to be "real" (ie, slanted RED lines in Figure-4) — with similar disturbance of the baseline in lead lead aVF (slanted BLUE lines) — albeit not in the other inferior lead ( = lead III), and not in other leads.

• I wondered IF the slanted RED lines in lead II might represent underlying AV dissociation?

To explore this possibility — I've isolated and enlarged in Figure-5 the 15 beats that we were seeing in Figure-4.

Figure-5: A closer look at the 15 beats in lead II.

As suggested earlier in Figure-2 — YELLOW arrows pointing to the terminal negative notching in Figure-6 highlight retrograde P waves. 

• But did YOU previously notice when you first examined this tracing, that this negative terminal notching is not present after beats #3 and 10? Why might this be so?

Figure-6: Retrograde P waves are not seen after beats #3 and 10.

Calipers are needed to answer this question.

• I thought the 2 consecutive RED arrows in Figure-7 looked to be highlighting 2 consecutive sinus P waves (ie, upright in this lead II rhythm strip).
• Setting my calipers to the P-P interval between these 2 consecutive RED arrows — I then looked for additional deflections likely to represent more sinus P waves, keeping in mind that slight variation in this P-P interval would be possible if there was an underlying sinus arrhythmia. This led me to the deflections highlighted by the PINK arrows in Figure-7.
• This left me to postulate the likely presence of "on time" sinus P waves directly over the QRS of beats #3 and 10 (the 2 WHITE arrows).
• NOTE: Beats #3 and 10 are the only QRS complexes in Figure-7 that lack retrograde conduction (ie, No YELLOW arrow is seen at the end of the QRS of beats #3 and 10).

Figure-7: Using calipers allows us to identify the likely presence of an underlying sinus rhythm (ie, AV dissociation).

My Proposed Laddergram:

Normally — I would never expect to see the simultaneous presence of AV dissociation from an underlying sinus rhythm in a patient with VT that produces 1:1 VA conduction. That said — this is what appears to be happening.

• I drew my proposed laddergram in Figure-8 — as my attempt to explain how these findings might reasonably account for the failure of retrograde conduction for only 2 out of 15 QRS complexes in this tracing.
• It is because the 2 "on time" underlying sinus P waves highlighted by the WHITE arrows in Figure-8 occur at precisely the time when ventricular beats #3 and #10 are conducting retrograde through the AV Node — that completion of retrograde conduction is rendered impossible by downward conduction from these 2 "on time" WHITE arrow P waves.
• PEARL #10 (Beyond-the-Core): This failure of retrograde conduction from ventricular beats #3 and 10 proves that today's rhythm is VT (and not SVT with aberrant conduction) even more convincingly than the finding of AV dissociation — because the reentry circuit of a supraventricular reentry rhythm could not be maintained if retrograde conduction was intermittent. (See Figures-5 and -6 and the accompanying text in ECG Blog #538 — for  explanation and illusration of the advanced concept of WHY intermittent retrograde conduction in association with a regular WCT rhythm  rules out a reentry SVT rhythm).
• Editorial Comment (Beyond-the-Core): I don't believe I have ever encountered the sequence of events portrayed in Figure-8. That said — the "beauty" of this rare occurrence is that: i) It provides a wonderful example of the concept known as "concealed" conduction — in which we are able to predict an electrophysiologic happening (in this case, failure of retrograde conduction after ventricular beats #3 and 10) despite not seeing the reason why this occurs on the surface ECG; — and, ii) It absolutely proves that today's ECG (and presumably most, if not all of the recurrent arrhythmia episodes this young woman has had) were the result of fascicular VT, and not of a reentry SVT.

Figure-8: My proposed laddergram.

CASE Conclusion:

I subsequently learned that this patient's recurrent ED visits for "palpitations" in association with a regular WCT rhythm (similar to the rhythm shown in today's case) — were resistent on several occasions to initial treatment with Adenosine, but responsive to IV Verapamil.

• This new historical information (ie, that several previous episodes responded to IV Verapamil, but not to IV Adenosine) — provides further support that this young woman's recurrent WCT episodes most likely were all the result of fascicular VT.
• And, now that the correct diagnosis of fascicular VT has been made — the patient was referred for EP study, most probably to be followed by ablation that hopefully will be curative.
• In the interim (awaiting scheduling for her EP appointment) — I'd consider oral Verapamil in hope of minimizing (eliminating) episodes.
• 
  
• P.S.: To answer the question posed by my title — Yes, some patients may become hypotensive with a reentry SVT rhythm (ie, If they have significant other problems that lower the BP — or if they have poor LV function — or if they fatigue after a prolonged period in a sustained SVT rhythm) — but many (most) patients maintain sufficient perfusion for even extended periods of time in a reentry SVT.

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

Acknowledgment: My appreciation to Hamdallah Naser (from AL-Najaf, Iraq) — for allowing me to use this case and this tracing.

================================== 

 

ADDENDUM:

I've added below relevant materials in support of today's diagnosis. 

Figure-9: QRS morphology in lead V1 suggestive of either aberrant conduction vs VT (Figure 08.25-1, excerpted from my ACLS Pocket Brain-2013).

Figure-10: Review of KEY features regarding Idiopathic VT (See text).

—  —

ECG Media PEARL #14 (8 minute Audio): What is Idiopathic VT? — with special attention to the 2 most common forms = RVOT (Right Ventricular Outflow Track) VT and Fascicular VT. 

ECG Blog #538 — An Unusual Finding

The ECG in Figure-1 was obtained from an adult who complained of frequent “palpitations”.  Imagine no history is available.

Choose the BEST Answer regarding the rhythm in Figure-1:

• a) The probability of VT is ~50%.
• b) The probability of VT is ~75%.
• c) The probability of VT is virtually 100%.
• d) The rhythm is a reentry SVT (ie, AVNRT or AVRT) with aberrant conduction.
• e) The rhythm is AFlutter with 2:1 AV conduction. 

Figure-1: The initial ECG in today's case — obtained from an adult with frequent "palpitations". (To improve visualization — I've digitized the original ECG using PMcardio).

My Initial Thoughts:

The rhythm in Figure-1 is a regular WCT (Wide-Complex Tachycardia) at ~160/minute, without clear sign of sinus P waves.

• As always, the diagnosis of VT must be considered until you prove otherwise — whenever you encounter a regular WCT rhythm without clear sign of sinus P waves.

Additional factors in favor of VT include the following:

• The frontal plane axis during the WCT rhythm is indeterminate (predominantly, but not completely negative in both leads I and aVF). This degree of frontal axis deviation favors VT — because it is not consistent with either LAHB (Left Anterior HemiBlock) or LPHB (Left Posterior HemiBlock) conduction. That said, because the frontal plane axis is not “extreme” (ie, not completely negative in either lead I or aVF) — this degree of axis deviation is suggestive but not diagnostic of VT (See Rule #1 and Table-2 in ECG Blog #42-bis, among many other examples throughout my ECG Blog of "extreme" axis deviation as a sign of VT).
• QRS morphology in lead V1 is all positive, but amorphous (ie, completely lacking in the triphasic rsR’ morphology characteristic of RBBB conduction). Although this lead V1 appearance does not completely rule out RBBB conduction (from either preexisting bundle branch block or rate-related aberrant conduction) — this QRS morphology does somewhat favor VT (as per Figure-2 in ECG Blog #42-bis). That said, wide terminal S waves are seen in left-sided leads I and V6 — and there is enough of a positive r wave in lead V6 such that RBBB conduction is still possible (ie, QRS morphology in Figure-1 is suggestive but not diagnostic of VT).
• 
  
• BOTTOM Line: At this point in our assessment — We lack a definitive answer. Without knowledge of this patient’s age, awareness of his/her prior medical history (ie, Any history of underlying heart disease?) — and without the benefit of a prior ECG that might reveal similar QRS widening during sinus rhythm — We are left with the statistical reality that the clear majority of regular WCT rhythms with atypical morphologic features and without clear sign of sinus P waves (as is the case in Figure-1) — are likely to be VT (although some of these regular WCT rhythms will turn out to be supraventricular).
• Looking again at the answer choices provided at the beginning of today’s post — the BEST choice would seem to be b) The probability of VT is ~75%.

BUT — There is One More Important Clue!

• HINT #1: This KEY clue that I have not yet mentioned tells us that the answer is not choice "b" — but something else. This KEY clue is related to atrial activity.

Take another LOOK at Today's Tracing in Figure-2:

• HINT #2: Why have I numbered the beats in Figure-2?

Figure-2: I've numbered the beats in today's tracing.

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

Answer: The Clue provided by Atrial Activity ...

It turns out that atrial activity is present in today's tracing — in the form retrograde P waves (highlighted by YELLOW arrows in Figure-3).

Figure-3: YELLOW arrows highlight retrograde P waves.

Retrograde P Waves:

Retrograde P waves typically appear as a negative notch or a negative deflection that occurs after the QRS in one or more of the inferior leads (ie, P wave negativity in the inferior leads being an indication that atrial depolarization is moving away instead of toward the AV Node).

• PEARL #1: The finding of AV dissociation during a regular WCT rhythm is an important clue that a regular WCT rhythm is the result of VT (as was shown in ECG Blog #133). But the finding of consistent 1:1 VA (retrograde) conduction is not AV "dissociation" — because in this case, each QRS complex is related to each neighboring QRS complex (ie, by a constant RP' interval). Both VT and reentry SVT rhythms may manifest consistent 1:1 VA conduction — such that the finding of 1:1 VA conduction during a regular WCT rhythm is of no assistance for distinguishing between VT vs an SVT rhythm (See ECG Blog #240 — for full discussion of the role that consistent 1:1 retrograde atrial activity may play in sustaining the reentry SVT rhythms of AVRT and AVNRT).
• 
  
• PEARL #2: In Figure-3, we do not see consistent 1:1 VA conduction — because retrograde P waves are not seen after each QRS complex (ie, There is no retrograde P wave seen after the QRS of beats #6, 12, 18 and 21 in Figure-3).

Looking Closer at Today's Retrograde Activity ...

To better visualize the nature of retrograde atrial activity in today's tracing — I've magnified in Figure-4 an excerpt of of beats #5-thru-15 from Figure-3.

• Can you appreciate what's happening to the RP' interval following beats #7-thru-12?

Figure-4: I've magnified beats #5-thru-15 from Figure-3. What's happening to the RP' interval following beats #7-thru-12?

Laddergram Illustration:

My laddergram in Figure-5 schematically shows that the RP' interval is progressively increasing as we move from beat #7 to beat #11 (dotted RED lines after these beats) — until we see that there is no retrograde P wave after beat #12.

• Retrograde conduction resumes after the brief pause between beats #12-13 — albeit once again with a shorter retrograde RP' interval after beat #13.
• PEARL #3: With this laddergram in Figure-5 — the YELLOW arrows represent retrograde P waves. Although subtle, the RP' interval is increasing. This is most easily appreciated by looking at the RP' interval before the retrograde Wenckebach conduction is blocked (darker BLUE double arrows seen in the rhythm strip after beat #11). Note subtle increase in the AV Nodal Tier in the angle of retrograde P wave conduction, that becomes maximal just before the P wave is dropped (dotted BLUE line in the AV Nodal Tier). And then, following the brief pause between beats #12-13 — the Wenckebach cycle begins again with the RP' interval shortening after beat #13. 

Figure-5: Laddergram showing retrograde Wenckebach conduction for magnified beats #5-thru-15 from Figure-4.

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

Significance of Intermittent Retrograde Conduction

In Figure-6 — I've drawn theoretical laddergrams to illustrate why the presence of intermittent retrograde conduction that does not disturb the regularity of a WCT rhythm is virtually diagnostic of VT (Roig et al — Circulation 153(15):1171-1173, 2026 — and — Pilecky et al — Eur Heart J 7:1-2, 2023).

• Panel A (Top laddergram in Figure-6) — A PAC (beat #3) is seen after 2 normal sinus beats. If the timing is "just right" — this PAC may initiate a reentry SVT rhythm (usually either AVNRT or AVRT). But because reentry SVT rhythms are dependent on continued retrograde conduction (dotted lines during the SVT run from beat #3-thru-11) — the reentry SVT will abruptly end if for any reason retrograde conduction fails (as it does here in this theoretical laddergram after beat #11).
• Panel B (Bottom laddergram in Figure-6) — Following 2 sinus beats, a run of VT begins with beat #3. I've drawn in some different possibilities for different VA conduction ratios. It should be apparent in Panel B that regardless if 1:1 VA conduction persists (as it does from beats #4-to-9) — or is intermittent with a 2:1 VA conduction ratio (as it is from beats #9-to-12) — or manifests retrograde Wenckebach conduction with progressive RP' prolongation until retrograde conduction fails (as occurs from beats #13-to-17) — the regularity of the VT rhythm is unaffected! This proves that ventricular activation is independent of atrial activity — thereby essentially confirming VT by eliminating the possibility of a reentry SVT that is dependent on persistence of retrograde conduction with a reentry circuit.

Figure-6: Theoretical laddergrams illustrating the expected effect of intermittent retrograde conduction on a reentry SVT vs the effect on VT.

================================= 

Final Thoughts on Today’s CASE:

Intermittent block of retrograde conduction during a regular WCT rhythm (be this by retrograde Wenckebach or other intermittent VA conduction phenomenon) — is not a common occurrence. This is an advanced concept that you will not often see. But it does occur (as in today's case) — and you can detect it if looked for.

• Going back to Figure-1 (and to Figure-3) — the fact that the WCT rhythm in today's case maintains a regular ventricular rate despite the failure to conduct retrograde with every beat essentially proves that this WCT rhythm is sustained VT (with the only rare exception being the possibility of a wide junctional tachycardia that conducts retrograde).

Clinically — this subtle informative clue of intermittent retrograde conduction during a regular WCT rhythm will usually not be needed to determine optimal initial management. 

• This is because IF your patient in a regular WCT rhythm without sinus P waves is hemodynamically unstable — then electrical cardioversion will be needed regardless of whether the rhythm is VT or an SVT.
• IF on the other hand, your patient in a regular WCT is stable — then a trial of medical therapy is reasonable. And, if you do recognize intermittent retrograde conduction despite maintenance of the regular WCT rhythm — then I'd skip a trial of Adenosine, because we would then know that the WCT rhythm is VT.

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

Acknowledgment: My appreciation to Khaled Elashiq, Hasan Al-Qassim and Mahmoud Al-Rahmoun (from Syria) for contributing this case.

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

 

 

ECG Blog #537 — What is the Rhythm?

The ECG in Figure-1 was obtained from an older woman with diabetes — who presented with acute dyspnea.

QUESTIONS:

• What is the rhythm?
• Is there an underlying RBBB (Right Bundle Branch Block) or aberrant conduction?

Figure-1: The initial ECG in today's case — obtained from an older woman with acute dyspnea. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on Today's CASE:

The above questions were contemplated by initial providers in today's case. As to the rhythm in Figure-1 — the KEY is to avoid being sidetracked, and instead to remain systematic in our approach to today's tracing.

• PEARL #1: Whenever I am confronted by a challenging 12-lead ECG in association with a challenging arrhythmia — I always favor first at least taking a brief look at the rhythm in the long lead rhythm strip. This is because many of the questions we might have about the 12-lead — will often be answered once we appreciate what the underlying rhythm is.

PEARL #2: When confronted with an arrhythmia that contains 2 or more different elements — Begin with the easier-to-interpret element(s). Doing so often renders interpretation of the more difficult elements much simpler to understand. Often, the 1st "easier-to-interpret" element that I address will be to determine IF there is an underlying rhythm?

• For example, in Figure-1 — the muliple different QRS shapes (that we see in the long lead II rhythm strip at the bottom of the tracing) are difficult to assess.
• As a result, I defer looking at QRS morphology in the long lead II — and instead, I begin my interpretation by looking to see IF there is an underlying rhythm? In other words — Do we see P waves in the long lead II?

What do YOU think?

• Do we see P waves in the long lead II?

• NOTE: The answer appears below in Figure-2.

 

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

Answer:

At 1st glance, on looking at the long lead II — I found it difficult to identify P waves until I arrived near the end of the rhythm strip.

• Then I saw the unmistakeable upright P wave in front of beat #17 (3rd RED arrow in Figure-2).
• And, once I saw this 1st upright P wave with a normal PR interval in front of beat #17 — it became easy to recognize the upright P wave in front of the next beat, albeit with a shorter PR interval (4th RED arrow in Figure-2).
• Now returning toward the front of the long lead II in Figure-2 — I was able to recognize the upright P waves (albeit with short PR intervals) in front of beats #7 and 8 (1st and 2nd RED arrows).

Figure-2: RED arrows in the long lead II rhythm strip highlight upright sinus P waves that I can readily identify.

Now take another LOOK at the long lead II in Figure-2. Can you identify any more P waves in this long lead rhythm strip?

• HINT: Use calipers! (Set your calipers to the P-P interval between any 2 consecutive P waves that we can readily identify = the P-P interval between either the first 2 — or the 3rd and 4th RED arrows in Figure-2).

• NOTE: The answer appears below in Figure-3.

 

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

Answer:

I've highlighted with PINK arrows in Figure-3 — a series of small, upright (partially hidden) deflections that represent underlying "on time" sinus P waves at an atrial rate of slightly more than 100/minute. 

• Isn't it logical for there to be additional "on time" sinus P waves that I've not yet labeled in Figure-3?

• NOTE: The answer appears below in Figure-4.

Figure-3: I've labeled with PINK arrows a series of additional partially hidden upright sinus P waves.

 

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

Answer:

It should now be apparent that an underlying rhythm of regular sinus P waves at a rate just over 100/minute is present throughout the entire long lead rhythm strip! My "color coding" in Figure-4 is as follows:

• The original 4 RED arrows represent the first 4 sinus P waves that were easiest to identify.
• PINK arrows in Figure-4 represent additional sinus P waves that I was able to identify by "walking out" the P-P interval that I had set my calipers to (Note partially hidden "on time" deflections highlighting the P waves under each of these PINK arrows).
• WHITE arrows in Figure-4 represent underlying "on time" sinus P waves that are all-but-certain to be present, albeit "hidden" by their simultaneous occurrence with either the QRS or T wave.
• 
  
• PEARL #3: Note that we have just established the presence of an underlying sinus P wave rhythm that for the most part is not related to neighboring QRS complexes. This is the definition of AV dissociation! — and the presence of AV dissociation during a regular wide tachycardia is virtually diagnostic of VT (See ECG Blog #133, among many other posts regarding the diagnostic value of AV dissociation). 

Figure-4: Colored arrows represent the underlying regular sinus rhythm that is present throughout today's tracing.

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

Putting It All Together ...

Now that we've established the presence of a regular underlying sinus P wave rhythm with some element of AV dissociation — We can take another look at the multiple QRS shapes in the long lead II rhythm strip.

• Note in Figure-5 that there are 4 upright QRS complexes (albeit with slight variation in shape between beats #6,7; and #16,17) — and that the remaining 15 beats manifest negative QRS complexes. 
• Note also that I've added the labels, "C" and "F" to the long lead II rhythm strip in Figure-5.
• The KEY is beat #17. The QRS complex of this beat #17 is the most narrow beat, as well as the beat that is preceded by the most normal PR interval. This suggests that beat #17 is being conducted!
• And, if beat #17 is sinus-conducted — whereas beats #1-thru-5; #8-thru-15; and #18,19 all look very different (all being predominantly negative) with AV dissociation — this must mean that these predominantly negative beats represent an ongoing, underlying ventricular rhythm, occurring here at a rate of ~115/minute.

PEARL #4: As discussed in a number of blog posts (See ECG Blog #108, among others) — an independent ventricular rhythm at a rate of less than 120-130/minute is probably best classified as AIVR (Accelerated IdioVentriclar Rhythm) rather than "VT" (Ventricular Tachycardia). This is important clinically — because AIVR is often a consequence of other ongoing events, such that AIVR does not necessarily mandate immediate treatment with cardioversion.

• PEARL #5: The reason today's rhythm is "tricky" — is that the 15 predominantly negative QRS complexes in the long lead II rhythm strip do not "look" wide! But if we look directly upward at simultaneously-recorded leads V1,V2,V3 — the all-upright monophasic R wave in lead V1 for beats #11-thru-14 clearly looks to be ventricular in etiology.
• Thus, this is not RBBB and not aberrant conduction. Instead — there is underlying AIVR at ~115/minute. We prove this by the presence of AV dissociation. 
• Beat #17 is a "Capture" beat (labeled "C" in Figure-5).
• The reason the QRS morphology of beats #6,7 and 16 all look slightly different than that of beat #17 — is that these other upright QRS complexes all manifest different degrees of "Fusion" (labeled "F" in Figure-5) — with the concept of fusion beats explained in ECG Blog #128.
• 
  
• PEARL #6: The importance of recognizing Fusion and Capture beats — is that in association with underlying AV dissociation, this proves beyond doubt that the 15 predominantly negative QRS complexes in Figure-5 are ventricular beats!

Figure-5: I've labeled "Capture" and "Fusion" beats.

CASE Conclusion:

Today's patient was an older woman with diabetes — who presented with acute dyspnea. And although I do not have the specific details of what happened — I advised the following regarding clinical management:

• AIVR is often a well tolerated rhythm that does not necessarily mandate antiarrhythmic treatment or immediate cardioversion IF the patient is hemodynamically stable.
• Thus, if the reason for this patient's acute dyspnea is something "fixable" (ie, acute heart failure) — it may be reasonable to treat the heart failure. This may be all that is needed for the AIVR to resolve on its own.
• I do not see evidence of an ongoing acute infarction in Figure-5. To assess this — I focused on ST-T wave morphology of the more normally conducted beats (ie, the capture and fusion beats #16,17 in simultaneously-recorded leads V5,V6 — and the fusion beats #6,7 in simultaneously-recorded lead aVF). These complexes suggested marked LVH (greatly increased R wave amplitude for beat #17 in leads V5,V6) with ischemic symmetric T wave inversion in beats #6,7 and 16,17 in simultaneously-recorded leads aVF,V5,V6 — but no ST elevation.
• BOTTOM Line: If this patient remained hemodynamically stable — it may be reasonable to treat her heart failure (or other treatable cause of her acute dyspnea) to see if normal sinus rhythm returned. Depending on how the patient did, as well as depending on serial ECG and Troponin results — a decision can be made as the patient stabilized as to whether cardiac catheterization or other intervention will be needed. 

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

Acknowledgment: My appreciation to Bashiruddin Sayeem  (from Chittagong, Bangladesh) for the case and this tracing.

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