ECG Blog #446 — What Kind of SVT?

You are shown the ECG in Figure-1 — told only that the patient had a “continuous" tachycardia.

QUESTIONS:

• How would YOU interpret the ECG in Figure-1?
• What is the differential diagnosis? — Treatment?

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 rhythm in Figure-1 — is a regular SVT (SupraVentricular Tachycardia) at a rate just under 150/minute, without clear sign of sinus P waves (ie, there is no upright P wave in lead II).

• The QRS is narrow in all 12 leads — which is why we know this is a supraventricular rhythm.
• Although sinus P waves are absent — there is atrial activity in the form of a negative deflection at a fixed interval distance from the QRS in each of the inferior leads (BLUE arrows in Figure-2).

Figure-2: I've labeled atrial activity in ECG #1 with BLUE arrows.

PEARL #1: The 3 main considerations regarding the nature of atrial activity highlighted by the BLUE arrows in Figure-2 are: i) Do these deep negative deflections that appear before the QRS in each of the 3 inferior leads represent retrograde P waves, being conducted backward from the preceding QRS complex; — ii) Or, do these negative deflections in the inferior leads represent forward-conducting P waves from an ectopic atrial site; — or, iii) Do these deflections represent junctional tachycardia?

• Depending on which of above considerations is operative — the differential diagnosis of the rhythm in ECG #1 will be between: i) A reentry SVT rhythm with retrograde atrial conduction; ii) ATach (Atrial Tachycardia); — or — iii) Junctional Tachycardia.
• It would seem in today's case, that an automatic junctional tachycardia is the least likely of the above 3 considerations — because the PR interval of these negative deflections before the QRS in each of the inferior leads is longer than the very short PR interval that I would expect if the rhythm was junctional tachycardia.
• But — the deflections highlighted by the BLUE arrows in Figure-2 certainly could represent an ectopic ATach.

PEARL #2: Retrograde atrial conduction is recognized by P wave negativity in the inferior leads (as a result of conduction moving away from the ventricles — and back toward the atria). Such retrograde conduction typically produces a positive P wave deflection in leads aVR, aVL, V1, and sometimes in lead V2 (See BLUE arrows in each of these leads in Figure-2).

• The above said — We still can not rule out the possibility that the mechanism of the rhythm in Figure-2 is an ectopic ATach.
• 
  
• The issue of reentry SVT rhythms was discussed in detail in ECG Blog #240. In that review, I emphasized that the most common form of reentry SVT is AVNRT of the "slow-fast" type, in which forward conduction occurs over the slower AV nodal pathway — with completion of the reentry circuit by conduction back to the atria over the faster AV nodal pathway. It is because this retrograde conduction (back to the atria) occurs over the faster AV nodal pathway — that retrograde P waves occur very close to the preceding QRS complex (either hidden, because they are contained within the preceding QRS complex — or with a very short RP' interval, with the retrograde P wave notching the end of the preceding QRS).
• Alternatively — when a portion of the reentry circuit is made up of an AP (Accessory Pathway) — the retrograde P wave will typically manifest a moderately long RP' interval (that occurs well after the QRS — usually within the latter part of the ST segment). Incorporation of a portion of the AP into the reentry circuit of an SVT rhythm constitutes AVRT. The RP' interval is moderately long — because it takes more time to complete this reentry circuit that is longer than the reentry circuit in AVNRT that is contained entirely within the AV node.

What is happening in today's case is different.

• IF the BLUE arrows in Figure-2 represent retrograde atrial conduction — then the RP' interval very long (taking up well over half of the R-R interval). As a result, if the BLUE arrows represent retrograde P waves — then this rhythm would be the atypical (and much less common) form of AVNRT, which is known as the "fast-slow" type (with forward conduction over the faster AV nodal pathway — and completion of the reentry circuit by conduction back to the atria over the slower AV nodal pathway).
• 
  
• BOTTOM Line: The principal differential diagnosis of the regular SVT rhythm in today's case is between: i) Atypical AVNRT of the "fast-slow" type; — vs — ii) Ectopic ATach.

PEARL #3: Distinction between atypical "fast-slow" AVNRT vs ectopic ATach can be difficult on the basis of a single ECG. Although in today's case — I thought the shape of the ST segment, and the very deep negative P waves in each of the inferior leads was more suggestive of atypical AVNRT — distinction between these 2 entities can sometimes only be made on EP testing.

• Look for the “Onset” (and/or Termination) of the Rhythm! — The KEY clue to the etiology of an SVT often lies with capturing either the beginning and/or the end of the SVT. 
• ATach often begins gradually, with progressive acceleration of the ectopic focus (ie, “warm-up” phenomenon). Then, there may be gradual slowing (ie, “cool-down”) of the rhythm as it ends. 
• In contrast — SVT reentry rhythms often start with 1 or more PACs that block conduction down one of the AV nodal pathways. This serves to immediately set up the reentry circuit, as the impulse starts down the other pathway. As a result — the onset of a reentry SVT is often abrupt (ie, accounting for the previous term used to designate this rhythm = PSVT = Paroxysmal SVT). The termination of reentry SVT rhythms is also usually quick (though this may occur over several beats).
• Unfortunately in today's case — the onset of the regular SVT in Figure-2 was not captured, so we are not privilege to this important clue.
• 
  
• NOTE: While our goal is to arrive at as precise of a rhythm diagnosis as possible — the "good news" is that for practical purposes — initial diagnostic and/or treatment measures in the field or in the ED for an undifferentiated regular SVT rhythm are similar (ie, consideration of a vagal maneuver — and/or use of an AV nodal blocking agent such as Verapamil/Diltiazem; a ß-Blocker, and possibly Adenosine).

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What Happens with "Fast-Slow" AVNRT?

To illustrate the mechanism of atypical "fast-slow" AVNRT — I show below in Figure-3 the laddergram discussed in ECG Blog #240.

• Starting with the normal sinus-conducted P wave ( = beat #3) — this is followed by a PAC ( = beat #4, which is recognized as a PAC because its P wave morphology differs from the sinus P wave that precedes beat #3).
• Mechanistically — if this PAC ( = beat #4) arrives at the AV node at just the right moment — it may encounter the slow AV nodal pathway at a point when this slow pathway is able to conduct retrograde (dotted line in the AV nodal tier of the laddergram that conducts back to the atria).
• And — if retrograde conduction over the slow pathway occurs at just the right moment — it may encounter the fast AV nodal pathway at a point when it is now able to conduct down to the ventricles. 
• In Figure-3 — these events initiate a reentry SVT of the "fast-slow" type for beats #4-thru-13. This reentry SVT stops after beat #13 — because this last beat in the run does not conduct retrograde! (ie, There is no negative P wave after beat #13).
• Sinus rhythm then resumes with beat #14 — but only lasts for 1 beat, because retrograde conduction of beat #14 is potentially able to initiate another run of SVT beginning with beat #15 (which we do not see — because the rhythm strip ends here).
• Now, if we go back to the start of this rhythm in Figure-3 — it looks as if another "fast-slow" run of AVNRT had just ended before beat #3.
• P.S. — Note that retrograde conduction from beat #4 is slightly faster (ie, with a slightly shorter RP' interval) than is retrograde conduction for all other beats on this tracing. Whether this reflects switch from one AV nodal pathway to another — or simply slowing of retrograde conduction after an initial beat is uncertain and, does not alter the finding that slow retrograde conduction (ie, with a long RP' interval) is the "substrate" for initiation and persistance of the fast-slow AVNRT in this patient.
• 
  
• PEARL #4: This less common form of "fast-slow" AVNRT that is illustrated in Figure-3 — has also been known as an "incessant" tachycardia. This name reflects that fact this atypical form of AVNRT is often difficult to treat because of its disturbing tendency of frequent recurrence and persistence once the reentry cycle is started. Presumably, the slower retrograde conduction back to the atria (that produces the very long RP' interval) — allows more time (and more opportunity) for forward conduction down the faster pathway to occur — and once this occurs, it tends to sustain the reentry cycle. (In contrast — "incessant" recurrence of reentry SVT is less likely with the typical "slow-fast" form of AVNRT, in which the shorter RP' interval allows less opportunity for the reentry cycle to be sustained).

Figure-3: Laddergram illustration of the mechanism for atypical "fast-slow" AVNRT (from ECG Blog #240). 

Editorial Comment: The intricacies of reentry SVT rhythms is a complex subject that I have simplified to facilitate practical understanding.

• For a more intricate analysis: See Katritsis and Josephson — Arrhythm Electrophys Rev 5(2):130-135, 2016.
• Additional easier-to-read links — Cadogan — Life-In-The-Fast-Lane, 2022 — and — Hafeez and Armstrong — StatPearls, 2023.

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The CASE Continues:

• The rhythm in today's case was treated with Adenosine. It finally responded to high-dose IV Verapamil.
• EP study confirmed that the mechanism of today's rhythm was AVNRT of the "fast-slow" type. Unfortunately — additional follow-up is not available. 
• Considering clinical options if this patient was ours to manage — the patient could be tried on a longterm AV nodal blocking agent (ie, oral Verapamil or Diltiazem; and/or a ß-Blocker) — but if unsuccessful (as is often the case with AVNRT of the fast-slow type) — referral to EP cardiology for consideration of ablation may become indicated.

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I did receive the 2 short rhythm strips in Figure-4 — that were recorded after IV Adenosine was given to today's patient.

QUESTION:

• What do YOU see?
• Are these rhythm strips consistent with the mechanism for fast-slow AVNRT that I illustrate in Figure-3?

Figure-4: Rhythm strips recorded after administration of IV Adenosine to today's patient.

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ANSWER = Figure-5:

I am not sure how long it was after IV Adenosine was given until the rhythm strips in Figure-5 were recorded. IDEALLY: A continuous rhythm strip should always be recorded for the 60-90 seconds after administration of IV Adenosine (as the BEST way to capture the critical diagnostic period prompted by this medication).

• The first 9 beats in Panel A of Figure-5 show a reentry SVT rhythm at ~135/minute, with a fairly long RP' interval (YELLOW arrows following these first 9 beats). Note slight slowing of the SVT with beats #8 and 9.
• Beat #10 is a PVC — after which a brief pause occurs.
• Beat #11 is a supraventricular escape beat — since it is not preceded by a sinus P wave. There is however a retrograde P wave (YELLOW arrow) following beat #11 — but note that the RP' interval following this beat is shorter than it was during the 9-beat run of AVNRT (That the RP' interval is decreasing is best appreciated by comparing the obviously longer RP' intervals following beats #1 and 2 — with this shorter RP' interval following beat #11).
• Beat #12 is another supraventricular escape beat. Note that no retrograde P wave follows this beat.
• Sinus conduction resumes with beats #13 and 14 (RED arrow) — with both of these sinus-conducted beats followed by retrograde P waves with a shorter RP' interval than was seen at the beginning of the AVNRT run for beats #1 and 2.
• 
  
• In Panel B — We now see normal sinus rhythm at a more appropriate rate, but now without retrograde conduction!
• Beat #7 is a PAC (occurring earlier-than-expected — and preceded by a different morphology P wave, as shown by the BLUE arrow). As was shown in Figure-3 — the onset of reentry SVT rhythms is often precipitated by one or more PACs that predispose to potential for the retrograde conduction that initiates and perpetuates the reentry cycle.

Putting It All Together:

These 2 short rhythm strips tell the story of how IV Adenosine successfully converted today's fast-slow AVNRT to sinus rhythm:

• The first 9 beats show the beginning of a slowing of this patient's AVNRT (that had been sustained as shown in Figure-1 at a rate closer to 150/minute). In additional to slowing of the reentry SVT rate — you'll often see introduction of slight irregularity into this previously regular rhythm (as we see in Panel A).
• You'll often see some ventricular beats (as per beat #10) as Adenosine is working. A series of escape beats often follows — as sinus rhythm resumes.
• As previously emphasized — it is the long RP' interval that characterizes (and sustains) this atypical fast-slow form of AVNRT. These 2 rhythm strips show the effect of Adenosine in reducing the RP' interval, with ultimate cessation of retrograde conduction.
• Normal sinus rhythm has returned in Panel B. The PAC (beat #7) no longer initiates a run of reentry SVT — because the AV node is no longer allowing retrograde conduction.

Figure-5: I've labeled Figure-4.

CASE Conclusion: 

As shown in Figure-5 — Adenosine converted the rhythm in today's case. But because of the ultra-short half life of Adenosine — the "incessant" fast-slow AVNRT rhythm kept returning until repeated IV Verapamil dosing succeeded in sustaining sinus rhythm.

• Figure-6 — shows that with the recording of ECG #3 — sinus rhythm has returned. Colored arrows highlight the change in P wave morphology between the 2 tracings.

Figure-6: Conversion to sinus rhythm following treatment.

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Acknowledgment: My appreciation to Kenneth Khoo (from Malasia) for the case and this tracing.

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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 #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. 
• ECG Blog #229 — Why is AFlutter so commonly overlooked?
• ECG Blog #137 — AFlutter with an unusual conduction ratio. 
• ECG Blog #138 — AFlutter vs Atrial Tachycardia. 
• ECG Blog #40 — Another regular SVT that turned out to be AFlutter.

• González-Torrecilla et al review distinction between AVNRT vs AVRT — in Ann Noninvasive Electrocardiol 16(1):85-95, 2011 .

Other sites where I've discussed similar cases:

• The March 6, 2020 post in Dr. Smith's ECG Blog.
• The October 31, 2016 post in Dr. Smith's ECG Blog.
• The October 16, 2019 post in Dr. Smith's ECG Blog. 
• 
  
• Please check out the November 12, 2019 post in Dr. Smith's ECG Blog — in which I reviewed the case of a different kind of regular SVT Rhythm (AFlutter). 

 

 

ECG Blog #445 — VT or LBBB?

The ECG in Figure-1 was obtained from an 80-year old woman — who presented to the ED (Emergency Department) — with a several hour history of "palpitations" and CP (Chest Pain). She was hemodynamically stable at the time ECG #1 was recorded.

QUESTIONS:

The ECG in Figure-1 was seen by a number of physicians — the majority of whom thought the rhythm was some form of SVT (SupraVentricular Tachycardia) with LBBB (Left Bundle Branch Block) aberration.

• Do YOU Agree with the interpretation of the majority of physicians who said that the rhythm in ECG #1 was SVT with LBBB aberration?
• How certain are you of your answer?
• How would you treat this patient?

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

MY Thoughts on Today's CASE:

The ECG in Figure-1 — shows a regular WCT (Wide-Complex Tachycardia) rhythm at a rate just under 150/minute, with no clear sign of sinus P waves.

• Although QRS morphology — is consistent with LBBB conduction in the limb leads of Figure-1 (ie, monophasic, all-upright R wave in lateral leads I and aVL) — QRS morphology is not as expected in the chest leads, because we never see a predominant R wave in lateral lead V6. Instead — a similar rS morphology is seen in all 6 chest leads, in which the initial upright deflection (r wave) is surprisingly wide already by lead V4. 
• NOTE: The deep S waves in leads V1,V2 in ECG #1 suggest the likelihood of underlying LVH. One reason why LBBB conduction in a patient with marked LVH may not evolve to a predominant (if not all positive) R wave by lead V6 — is that leftward and posterior forces of marked LVH with LBBB may delay transition to predominant positivity in the chest leads until more posteriorly oriented chest leads, such as V7 or V8.

MY Impression of ECG #1: As emphasized often in this ECG Blog (See today's ADDENDUM below) — statistical odds that a regular WCT rhythm without clear sign of sinus P waves will turn out to be VT begin at 80% likelihood. 

• The older age of today's patient and somewhat atypical QRS morphology for LBBB conduction — move this statistical likelihood up to ~90%.
• While 90% is not equal to 100% — the message regarding the ECG in Figure-1 is clear: Assume VT until proven otherwise! Treat the patient accordingly.
• PEARL #1: Stated a different way — Rather than having to prove that ECG #1 is VT — We need to prove that this rhythm is not VT. Until we do — Assume VT until proven otherwise (and treat the patient accordingly).

Additional Points regarding ECG #1: 

Is there truly no sign of atrial activity in this initial tracing?

• Although there are small-amplitude undulations in the baseline in today's initial tracing — these undulations are present in all 6 limb leads, whereas "true" atrial activity will generally appear more prominently in some leads compared to others (and true atrial activity should not persist throughout the entire baseline — as we see in leads I, aVR and aVL).
• The undulations that we see in the limb leads of Figure-1 — are not consistent in shape, as I would expect them to be if this truly represented atrial activity.
• Finally — although the rate of almost 150/minute in ECG #1 should suggest the possibility of underlying AFlutter with 2:1 AV conduction — 2:1 atrial activity does not work out! (See Figure-2):

Figure-2: I've added RED lines to Figure-1 to show that 2:1 atrial activity does not work out! (See text).

PEARL #2: The way in which I look for flutter waves is to carefully set my calipers at precisely HALF the R-R interval of the tachycardia (since IF the rhythm is AFlutter — then the atrial rate should be twice the ventricular rate if there is 2:1 AV conduction). 

• My "GO TO" leads that I favor for identifying less obvious atrial activity are leads II, III, aVF; aVR; and V1. IF none of these 5 leads suggest atrial activity — then I’ll survey the remaining 7 leads. That said, AFlutter will almost always provide ready evidence of atrial activity in one or more of my “Go To” leads.
• In Figure-2 — I've placed RED lines above those points in leads II, III and aVR that I thought might possibly indicate underlying atrial activity. But notice that the distance between these RED lines is not constant, as it would need to be IF there was underlying flutter with a precisely regular P-P interval. Therefore — the rhythm in ECG #1 is not AFlutter! (See ECG Blog #287 — if interested in more on ECG recognition of AFlutter).

How Would You Treat this Patient?

As is often emphasized in this ECG Blog — "Sometimes ya just gotta be there!" That said — I'll offer the following thoughts:

• The rhythm in ECG #1 is a regular WCT rhythm at ~150/minute, without clear sign of sinus P waves. As noted above, given the older age of this patient and the somewhat atypical QRS morphology for lbbb conduction — I would estimate statistical likelihood that the rhythm is VT at ~90%. Therefore — Assume VT, and treat accordingly!
• We are told that this patient was "hemodynamically stable" — but, given that this older woman is complaining of chest pain — I would not want to leave this patient in this rhythm (that is probably VT) for an extended period of time before moving to synchronized cardioversion.
• I would not try Adenosine — because the rhythm is most likely ischemic VT, and: i) Although Adenosine may convert some forms of idiopathic VT (ie, in which the patient is a younger adult without underlying heart disease) — Adenosine is unlikely to convert ischemic VT; and, ii) Adenosine is not completely benign (For more on the pros and cons of Adenosine — See the ADDENDUM in ECG Blog #393).
• Depending on your level of comfort in this particular case (ie, "Sometimes ya just gotta be there!" ) — IV Amiodarone might be tried, with the provider being ready to cardiovert at the 1st sign of decompensation.

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The CASE Continues:

The patient spontaneously converted to the repeat ECG that is shown below in Figure-3. This spontaneous conversion occurred before any antiarrhythmic medication was given.

• The patient was placed on a "Rule-Out MI" protocol — but the CP she was having disappeared almost immediately after she spontaneously converted to the rhythm shown in ECG #2.
• IV Amiodarone was started in the hope of preventing recurrence of the WCT that the patient presented with.

QUESTIONS:

• How would YOU interpret the repeat ECG shown in Figure-3?
• Is the rhythm in ECG #2 now sinus?
• Does the ECG in Figure-3 alter your opinion in any way as to what the initial rhythm in Figure-1 was?
• Is the patient having an acute MI?

Figure-3: I have put together the initial ECG — with the repeat ECG obtained after spontaneous conversion. (To improve visualization — I've digitized the original ECG using PMcardio).

ANSWERS:

Looking at ECG #2 — the rate of the rhythm has slowed and the QRS complex has narrowed compared to what it was in ECG #1. That said — Did YOU Notice that no upright P wave is present in lead II of ECG #2? (BLUE arrow in lead II of Figure-4).

• PEARL #3: The lack of a clearly upright P wave in lead II in the presence of upright P waves in leads I and aVL (RED arrow in Figure-4) — is most often due to 1 of 2 causes: i) A low atrial rhythm; — or, ii) A "technical misadventure". 
• The most common type of lead reversal is mixup of the LA (Left Arm) and RA (Right Arm) electrodes. This is not present in ECG #2 because the P wave and QRS complex are both positive in lead I, and the QRS is negative in lead aVR (See ECG Blog #264 — for more on LA-RA reversal).
• 
  
• The 2nd most common type of lead reversal in my experience, is mixup of the LA-LL (Left Arm - Left Leg) electrodes (See ECG Blog #375 — for more on LA-LL reversal).
• The "good news" — is that regardless of whether there is a low atrial rhythm in ECG #2 — or, whether the rhythm is sinus, but with LA-LL lead reversal — the patient is no longer in a WCT. Instead — the patient has spontaneously converted to a supraventricular rhythm at a much more controlled heart rate (and without suggestion of acute ST-T wave changes in this repeat ECG).

Figure-4: I've added colored arrows to ECG #4 to highlight the lack of an upright P wave in lead II of the post-conversion tracing.

IF there was LA-LL Reversal — What would ECG #2 Look Like?

Lead placement was not checked after recording the post-conversion tracing — and I was not provided with any more tracings from this case. As a result — We'll never know if the post-conversion tracing represents a low atrial rhythm or sinus rhythm with LA-LL reversal.

• As discussed and illustrated in ECG Blog #375 — LA-LL lead reversal will result in the ECG changes shown in Figure-5.

Figure-5: The effect of LA-LL reversal on an ECG.

Correcting for LA-LL Reversal:

We can correct for the predicted changes of LA-LL lead reversal. Doing so allows us to predict what the post-conversion ECG would have looked like if the reason for the lack of an upright P wave in lead II of ECG #2 was LA-LL reversal.

• I show in ECG #2a (Bottom tracing in Figure-5) — what the post-conversion ECG would have looked like if the reason for lack of an upright P wave in lead II was LA-LL reversal.
• 
  
• Note in ECG #2a — that an upright sinus P wave is now seen in lead II (as would be expected if the post-conversion rhythm is sinus).

So — Assuming that there was LA-LL lead reversal in ECG #2 — that we have now "corrected for" in ECG #2a — I show in Figure-6 what comparison of today's initial tracing ( = ECG #1, in which there was the regular WCT rhythm) would look like — compared to the post-conversion tracing corrected for presumed LA-LL lead reversal.

Figure-6: What ECG #2 would have looked like if the reason for the lack of an upright P wave in lead II was LA-LL reversal.

PEARL #4: The reason for me highlighting the likelihood of LA-LL reversal in the post-conversion tracing of today's case — is that we will often not be certain as to the etiology of a regular WCT at the time that we need to begin treatment.

• In such cases — it may only be after return to sinus rhythm, that by comparison of the WCT with the post-conversion tracing, can we retrospectively determine whether the WCT was VT (See ECG Blog #422 and ECG Blog #263).
• In today's case — the corrected post-conversion tracing ( = ECG #2a) shows sinus rhythm and no preexisting bundle branch block. While this does not rule out the possibility of rate-related aberrant conduction — the unusual QRS morphology that I described above still suggests (in my opinion) — a ~90% probability that the regular WCT in ECG #1 was VT.

CASE Conclusion:

Given the rapid rate of the regular WCT rhythm in today's case in this symptomatic older woman — additional evaluation to assist in optimal management was indicated.

• Echo was done — and was found to be unremarkable (with normal LV function). 
• Troponin — was negative for acute infarction. 
• Cardiac cath — showed no significant coronary disease.
• The patient was offered EP (ElectroPhysiologic) study — but she refused, since she "was feeling well". She was discharged from the hospital on Amiodarone.

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Acknowledgment: My appreciation to Jean Max Figueiredo (from Nova Iguaçu, Brazil) for the case and this tracing.

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ADDENDUM (8/29/2024):

• I've reproduced below from ECG Blog #196 — a number of helpful figures and my Audio Pearl on assessment of the regular WCT rhythm.

Figure-7 : My LIST #1 = Causes of a Regular WCT (Wide-Complex Tachycardia) of uncertain Etiology (ie, when there is no clear sign of sinus P waves).

Figure-8: Use of the "3-Simple Rules" for distinction between SVT vs VT.

Figure-9: Use of Lead V1 for assessing QRS morphology during a WCT rhythm.

—  —

ECG Media PEARL #13a (12:20 minutes Audio) — reviews “My Take” on assessing the regular WCT (Wide-Complex Tachycardia), when sinus P waves are absent — with tips for distinguishing between VT vs SVT with either preexisting BBB or aberrant conduction.

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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.
• 
  
• 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. 
• 
  
• ECG Blog #220 — Review of the approach to the regular WCT ( = Wide-Complex Tachycardia).
• e Regular WCT (Wide-Complex Tachycardia).
• ECG Blog #196 — Reviews another Case with a regular WCT rhythm.
• ECG Blog #263 and Blog #283 — Blog #361 — and Blog #384 — More WCT Rhythms ...
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• ECG Blog #197 — Reviews the concept of Idiopathic VT, of which Fascicular VT is one of the 2 most common types. 
• ECG Blog #346 — Reviews a case of LVOT VT (a less common idiopathic form of VT).
• 
  
• 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 #301 — Reviews a WCT that is SupraVentricular! (with LOTS on Aberrant Conduction).
• 
  
• 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 — Criteria to distinguish VT vs Aberration.
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• ECG Blog #133 and ECG Blog #151— for examples in which AV dissociation confirmed the diagnosis of VT.

• Working through a case of a regular WCT Rhythm in this 80-something woman — See My Comment in the May 5, 2020 post on Dr. Smith’s ECG Blog. 
• Another case of a regular WCT Rhythm in a 60-something woman — See My Comment at the bottom of the page in the April 15, 2020 post on Dr. Smith’s ECG Blog. 
• 
  
• Review of the Idiopathic VTs (ie, Fascicular VT; RVOT and LVOT VT) — See My Comment at the bottom of the page in the September 7, 2020 post on Dr. Smith’s ECG Blog.
• Review of a different kind of VT (Pleomorphic VT) — See My Comment in the June 1, 2020 post on Dr. Smith’s ECG Blog.

 

ECG Blog #444 — CP and Aberrant SVT?

The ECG shown in Figure-1 — was obtained from an older man with “CP” (Chest Pain) for the past 2 days. BP = 80/50 mm/Hg. Adenosine 6 mg IV was tried without response.

QUESTIONS:

• How would YOU interpret this ECG? 
• Your thoughts regarding optimal management?

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

MY Initial Thoughts on Today's ECG:

The ECG in Figure-1 — shows what I initially thought was a regular WCT (Wide-Complex Tachycardia) at ~180/minute, without clear sign of of atrial activity.

• My initial thoughts were that statistically — knowing nothing more than that this older man is presenting in a WCT rhythm that looks regular, and that lacks clear sign of atrial activity — the chance that the rhythm in Figure-1 is VT (Ventricular Tachycardia) is at least 80%.
• Looking closer at the ECG in Figure-1 — QRS morphology does not resemble any known form of conduction defect because: i) Although the all positive QRS complex in lead V1 could represent some form of RBBB (Right Bundle Branch Block) — the amorphous shape of this V1 complex (ie, without any hint of the expected triphasic configuration that is typical for RBBB conduction) — this amorphous shape of the QRS in lead V1 favors VT (within the BLUE rectangle in Figure-2); — ii) The almost all negative QRS in lead I suggests a marked right axis much more consistent with VT (within the RED rectangle in Figure-2); — iii) Abrupt transition from the predominant positivity seen from lead-V1-until-lead-V5 — to sudden development of predominant negativity in lead V6 strongly favors VT (within the other BLUE rectangle); — and, iv) The initial deflection of the QRS in multiple leads is slow (especially for the overly wide small initial r waves in leads I and V6) — with slow initial depolarization of the QRS in multiple leads suggesting origin in the ventricles (ie, away from the conduction system — therefore most likely to be VT).
• Putting this All Together (ie, considering older age of this patient and complete lack of resemblance to any known form of conduction defect) — I now estimated statistical likelihood of VT at over 90%.

BOTTOM Line: Although I would not yet be 100% of the etiology of today’s initial rhythm — what is certain, is that immediate treatment is needed!

• Given 90+% likelihood that the rhythm in Figure-2 is VT — We need to assume VT until proven otherwise (and treat the patient accordingly!).
• As noted above — 1 dose of Adenosine was tried without success. That said — this would not be a patient for whom I would try Adenosine because: i) Although Adenosine may successfully convert some forms of idiopathic VT (ie, VT in a patient who does not have underlying heart disease — as discussed in ECG Blog #197) — Adenosine is not effective for treating ischemic VT — which this older patient with markedly abnormal QRS morphology almost certainly has; ii) Adenosine is not a completely benign medication (See ECG Blog #402 for pros and cons of using Adenosine); and, iii) This patient is symptomatic. He also appears to be hemodynamically unstable (ie, The patient has had CP for 2 days — the rate of the initial rhythm in Figure-2 is rapid — and the patient's BP at the time this rhythm was recorded = 80/50 mm Hg.). 
• Instead — immediate cardioversion is indicated! Given that this patient is symptomatic (as well as hemodynamically unstable) — it no longer matters whether this rhythm is of supraventricular etiology or VT because regardless — immediate cardioversion is clearly indicated.

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PEARL #1: I will emphasize that although it may seem that my above step-by-step discussion of how I assessed ECG #1 is complex — the total time it took me to arrive at the greater than 90% likelihood of VT was less than 10 seconds. With practice — this becomes easy to do. But for those wanting a "simpler" approach" — Consider the following (which I review below in my ADDENDUM):

• This patient is in a wide, "ugly-looking" and seemingly regular tachycardia without P waves.
• As per Figures-5, -6, and -7 below in the ADDENDUM — there is marked right axis — the QRS is almost all negative in lead V6 — and the amorphous upright QRS in lead V1 does not look anything like a typical RBBB pattern, which characteristically manifests a triphasic (rSR' complex) in lead V1.
• And — the patient is older — has been having CP — and is hypotensive (80/50 mm Hg). Therefore, this rhythm has to be assumed VT until proven otherwise — and — in need of immediate cardioversion (regardless of what the rhythm turns out to be).

Figure-2: I've labeled the KEY leads that "caught" my eye (See text).

CONFESSION: I initially thought the WCT rhythm in Figure-2 was regular. It turns out that today's initial rhythm is not regular (This is perhaps best seen in lead V3 — which suggests an almost alternating regularity between an ever-so-slightly longer vs a slightly shorter R-R interval).

• As opposed to polymorphic VT that by definition is irregularly irregular — monomorphic VT is usually a fairly (if not completely) regular rhythm (See ECG Blog #231 for the various forms of VT).
• Most of the time when a monomorphic WCT rhythm is not regular — the rhythm will be of supraventricular etiology with either preexisting bundle branch block or a rate-related form of aberrant conduction.
• 
  
• PEARL #2: The above said — there are 2 common exceptions to the generality that monomorphic VT is usually a regular rhythm. These exceptions are IF: i) There is a "warm-up" period of slower and gradually accelerating ventricular beats before the VT becomes regularized; — or, ii) There is a "cool-down" period in which after the regular run of VT, the rate of the VT progressively slows until VT run finally resolves (these concepts thoroughly illustrated and explained in ECG Blog #417).
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• PEARL #3: Aside from a "warm-up" and/or "cool-down" period just before or just after a run of regular monomorphic VT — On occasion, monomorphic VT may simply manifest a variable R-R interval (Oreto et al — Am Heart J 124(6):1506-11, 1992). Potential reasons for R-R interval variability with monomorphic VT include: i) The presence of 2 VT reentry circuits that share the same exit pathway; or, ii) Variation in conduction velocity over the reentry circuit.
• Bottom Line — Most of the time (but not always) — monomorphic VT will be regular. But if a run of wide beats without P waves is not regular, this finding alone does not necessarily rule out the possibility of VT.

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The CASE Continues: 

Following 1 dose of Adenosine — synchronized cardioversion was applied. The result is shown in Figure-3.

QUESTION:

• How would YOU interpret the post-cardioversion ECG?

Figure-3: The repeat ECG recorded after synchronized cardioversion of the rhythm in Figure-2. (To improve visualization — I've digitized the original ECG using PMcardio).

The Post-Cardioversion ECG in Figure-3:

Although the presence of much artifact in Figure-3 makes assessment more difficult — this post-cardioversion tracing is interpretable:

• The "good news" — is that sinus rhythm has been restored, as noted by the presence of upright P waves with fixed and normal PR interval in lead II.
• All intervals (PR-QRS-QTc) and the frontal plane axis are normal. There is no chamber enlargement.
• There is low voltage in all 6 of the limb leads (More on this momentarily).

Regarding Q-R-S-T Changes: 

• There is a Q wave in lead III.
• R wave progression is not normal. Instead — the R wave is already predominant (R>S wave) in lead V1. As reviewed in ECG Blog #81 — the finding of a Tall R Wave in Lead V1 should prompt consideration of 6 potential entities (More on the likely cause of the Tall R in V1 in today's case momentarily).

Regarding ST-T Wave Changes (See Figure-4):

• Although there is much artifact-related variation in ST-T wave morphology — all 3 of the inferior leads (within the RED rectangles in leads II,III,aVF) show hyperacute ST elevation, in which T waves in these leads dwarf the tiny QRS complexes.
• That this inferior lead ST elevation is "real" and acute — is confirmed by the mirror-image opposite picture of hypervoluminous T wave inversion in high-lateral leads I and aVL (as per the BLUE arrows in these leads).

In the Chest Leads:

• My "eye" was immediately captured by the marked ST depression in leads V1,V2 (within the RED rectangle) — with these first 2 chest leads showing disproportionately tall (predominant) R waves.
• Finally — lateral chest lead V6 shows coved ST elevation (within the BLUE rectangle in this lead).

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Putting It All Together: 

Keeping in mind that today's patient was just cardioverted out of sustained VT — We need to contemplate WHY might this patient have been in VT?

• PEARL #4: As alluded to above — the finding of a Tall R Wave in Lead V1 should prompt consideration of the following LIST of the 6 most common Causes: i) WPW; ii) RBBB; iii) RVH; iv) Posterior MI; v) HCM (Hypertrophic CardioMyopathy); and, vi) Normal variant — as a diagnosis of exclusion (See ECG Blog #81 for more on this issue). 
• Working through the above LIST — the narrow QRS complex rules out WPW and RBBB — there are no findings suggestive of chamber enlargement — an Echo would rule out HCM — and ECG #2 is clearly not a normal variant. This leaves posterior MI as the most likely cause of the Tall R in Lead V1 of ECG #2.
• 
  
• PEARL #5: A LIST of causes of low voltage is reviewed in ECG Blog #272 — of which reduced cardiac output as a result of myocardial "stunning" in association with a large acute MI is the important consideration in today's case.
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• BOTTOM Line: The ECG in Figure-4 shows an extensive infero-postero-lateral STEMI. The early transition in the chest leads (ie, with predominant R wave already in lead V1) — is the mirror-image equivalent of a Q wave, and is consistent with posterior infarction. If the dramatically reduced limb lead voltage is a new finding — it most likely represents reduced cardiac output from extensive infarction. Prompt cath is clearly indicated. Unfortunately — further follow-up in today's case is not available.

Figure-4: I've labeled KEY findings in the post-conversion ECG.

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Acknowledgment: My appreciation to Rajeesh R Pillai (from Kollam, India) for the case and these tracings.

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ADDENDUM (8/23/2024):

• I've reproduced below from ECG Blog #196 — a number of helpful figures and my Audio Pearl on assessment of the regular WCT rhythm.

 

Figure-5 : My LIST #1 = Causes of a Regular WCT (Wide-Complex Tachycardia) of uncertain Etiology (ie, when there is no clear sign of sinus P waves).

Figure-6: Use of the "3-Simple Rules" for distinction between SVT vs VT.

Figure-7: Use of Lead V1 for assessing QRS morphology during a WCT rhythm.

—  —

ECG Media PEARL #13a (12:20 minutes Audio) — reviews “My Take” on assessing the regular WCT (Wide-Complex Tachycardia), when sinus P waves are absent — with tips to distinguish between VT vs SVT with either preexisting BBB or aberrant conduction.

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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.
• ECG Blog #205 — Reviews my Systematic Approach to 12-lead ECG Interpretation.
• 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 — Another Case with a regular WCT rhythm.
• ECG Blog #263 and Blog #283 — and Blog #361 — More WCT Rhythms ...
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• ECG Blog #197 — Reviews the concept of Idiopathic VT, of which Fascicular VT is one of the 2 most common types. 
• ECG Blog #346 — Reviews a case of LVOT VT (a less common idiopathic form of VT).
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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, the Hemiblocks — and  the Bifascicular Blocks.
• ECG Blog #211 — WHY does Aberrant Conduction occur?
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• ECG Blog #42 — Review of criteria to distinguish between VT vs Aberration.

• Working through a case of a regular WCT Rhythm in this 80-something woman — See My Comment in the May 5, 2020 post on Dr. Smith’s ECG Blog. 
• Another case of a regular WCT Rhythm in a 60-something woman — See My Comment at the bottom of the page in the April 15, 2020 post on Dr. Smith’s ECG Blog. 
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• Review of the Idiopathic VTs (ie, Fascicular VT; RVOT and LVOT VT) — See My Comment at the bottom of the page in the September 7, 2020 post on Dr. Smith’s ECG Blog.
• Review of a different kind of VT (Pleomorphic VT) — See My Comment in the June 1, 2020 post on Dr. Smith’s ECG Blog.

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• ECG Blog #193 — Reviews the basics for predicting the "culprit" artery (as well as reviewing why the term "STEMI" — should be replaced by "OMI" = Occlusion-based MI).

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• CLICK HERE — for my 6 new ECG Videos (on Rhythm interpretation — 12-lead interpretation with Case Studies for ECG diagnosis of acute OMI).
• CLICK HERE — for my 2 new ECG Podcasts (on ECG & Rhythm interpretation Errors — and — Errors in assessing for acute OMI).

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• Recognizing hyperacute T waves — patterns of leads — an OMI (though not a STEMI) — See My Comment at the bottom of the page in the November 8, 2020 post on Dr. Smith's ECG Blog.
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• ECG Blog #351 — Blog #285 — Blog 246 — Blog #80 — for examples of acute posterior OMI.