Sunday, May 2, 2021

ECG Blog #220 (ECG MP-37) — VT or Aberrancy?


The long lead II rhythm strip shown in Figure-1 was obtained from an 51-year-old man who presented to the ED (Emergency Department) with "palpitations" that began 1 hour earlier.

  • HOW would you interpret this tracing?
  • Clinically — What would YOU do?


Figure-1: Long lead II rhythm strip, obtained from an 51-year-old man with palpitations (See text).


 

 

 

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NOTE #1: Some readers may prefer at this point to listen to the 6:00 minute ECG Audio PEARL before reading My Thoughts regarding the ECG in Figure-1. Feel free at any time to review to My Thoughts on this tracing (that appear below ECG MP-37).

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Today’s ECG Media PEARL #37 (6:00 minutes Audio) — Reviews how to determine IF Your Patient with an Arrhythmia is Hemodynamically Stable!

 

 

MY Approach to the Rhythm in Figure-1:

We are provided with only very limited clinical information — namely, that the patient is a 51-year-old man who presented to the ED with "palpitations" of 1-hour duration. Clearly, we need to find out more about what is going on ...

  • The 1st Thing to do — is to LOOK at the patient! The KEY Question to answer is to determine IF the patient is hemodynamically stable! 
  • The above 6-minute Audio PEARL ( = ECG MP-37addresses this issue in detail. In essence — "Ya gotta be there!" in order to determine if the patient is hemodynamically stable (ie, without significant symptoms such as chest pain, shortness of breath, hypotension, mental status changes — as a direct result of the fast rate).
  • The importance of assessing for hemodynamic stability, even before deciding on the rhythm diagnosis — is that IF the patient is not hemodynamically stable with the rhythm shown in Figure-1 — then it no longer matters whether this rhythm is VT (Ventricular Tachycardia)  or an SVT (SupraVentricular Tachycardia)  or something else — since regardless, immediate synchronized cardioversion will be indicated!
  • On the other hand — IF the patient is hemodynamically stable with the rhythm in Figure-1, then by definition there is at least a moment-in-time for you to assess the rhythm diagnosis.

 


For the purpose of discussion — Let's assume that this patient is and remains hemodynamically stable!

 

  • QUESTION: IF this patient is hemodynamically stable — Does this rule out the possibility that the rhythm is VT?

 

 

 

ANSWER:

  • Definitely not! Although many patients with sustained VT promptly lose consciousness — a surprising number of patients in sustained VT remain alert and relatively asymptomatic for not only minutes — but sometimes for hours or longer (I am aware of a significant number of cases of sustained VT lasting over a day).
  • PEARL #1: The fact that a patient is alert, with a normal (or even increased) blood pressure and no more than minimal symptoms — does not rule out the possibility of VT.

 

 

What NEXT

  ( assuming the patient remains hemodynamically stable)?

 

 

ANSWER:

Since the patient is hemodynamically stable — it's time to assess the rhythm in Figure-1. I favor the Ps, Qs & 3R Approach (Reviewed in ECG Blog 185).

  • P waves are absent on this single lead monitoring strip.
  • The QRS is wide. Although the QRS complex does not look to be excessively wide — it clearly takes up at least 60% of 1 large box (shown in PURPLE in Figure-2) — which means that QRS duration is ≥0.12 second.
  • Regularity: The rhythm is regular.
  • Rate: The rate is rapid. Figure-2 illustrates use of the Every-Third-Beat Method for rapid estimation of heart rate (this method discussed in full in ECG Blog #210). It takes a little less than 5 large boxes (BLACK numbers in Figure-2) — to record 3 beats (RED numbers). Therefore — 1/3 of the rate is a bit faster than 300 ÷ 5 = 60-65/minute X 3 ~190-195/minute as the ventricular rate.
  • Related: Since P waves are absent — there is no "relation" between P waves and the QRS.
  • Therefore — We have described the rhythm in Figure-2 as a regular WCT ( = Wide-Complex Tachycardia) at ~190/minute, without clear sign of atrial activity.

 

Figure-2: I've labeled Figure-1 to illustrate estimation of heart rate (by the "every-third-beat" Method) — and — assessment of QRS duration (the solid PURPLE box showing that onset and offset of the QRS measures at least 0.12 second).


 

QUESTIONS:

  • What is the differential diagnosis of the regular WCT rhythm in Figure-2?
  • What can we do to increase the accuracy of our diagnosis?




ANSWERS:

I favor considering the following 10 entities in the Differential Diagnosis of a Regular WCT rhythm, in which P waves are absent:

  • VT (Ventricular Tachycardia).
  • VT
  • VT
  • VT
  • VT
  • VT
  • VT
  • VT
  • An SVT (SupraVentricular Tachycardia) with either preexisting BBB (Bundle Branch Block) or Aberrant Conduction.
  • Something else ... (ie, WPW, hyperkalemia).

 

 

 

KEY POINTS Regarding the Above Differential Diagnosis:

  • My reason for repeating VT no less than 8 times before listing another possibility — is to emphasize that statistical odds that a regular WCT rhythm without clear sign of atrial activity will turn out to be VT begin at ~80%. As per ECG Blog #196 — these odds increase to ≥90% if the patient is of a "certain age" (ie, middle-aged and beyond) and has underlying heart disease. As a result — Assume VT until proven otherwise! 
  • PEARL #2: When assessing a hemodynamically stable patient in a regular WCT rhythm without P waves — our "mindset" should be that we need to prove that the rhythm is not VT, rather than the other way around.

 


Regarding the Next Thing To Do:

  • Since we are told that this patient remains hemodynamically stable — the next thing to do is obtain a 12-lead ECG during the tachycardia (Figure-3):

 

Figure-3: 12-lead ECG obtained from an 51-year-old man with palpitations (See text).


 


 

 

Reasons for Getting a 12-Lead During the Tachycardia:

As alluded to in ECG Blog #196 — there are a number of reasons for obtaining a 12-lead ECG duringthe wide tachycardia:

  • Getting a 12-lead allows for assessment of QRS morphology. This 12-lead tracing may prove to be diagnostic of either VT or a supraventricular etiology (See Figure-6 and Figure-7 in the ADDENDUM below).
  • Getting a 12-lead provides us with 11 additional leads to look for atrial activity. This may reveal "telltale" flutter waves with 2:1 AV conduction — or, it may uncover previously hidden regular sinus P waves that are totally dissociated from neighboring QRS complexes, thereby proving that the rhythm is VT.
  • IF there is any doubt about QRS duration — assessing the QRS complex in all 12 leads should resolve the problem. Sometimes, a part of the QRS lies on the baseline in one or more lead — and, if this happens in the one lead you are monitoring — it may make the QRS appear much narrower than it really is.
  • Assessing frontal plane axis during a regular WCT rhythm is EASY to do and, may be diagnostic. IF there is "extreme" axis deviation (as determined by the finding of an all negative QRS in either lead I or in lead aVF— this strongly suggests that the rhythm is VT.
  • Sometimes, definitive diagnosis of a regular WCT rhythm will not be possible during the tachycardia. However, in some of these cases — comparing the 12-lead ECG obtained during tachycardia with a follow-up ECG obtained after conversion to sinus rhythm may allow retrospective diagnosis of the WCT rhythm.
  •  
  • PEARL #3: In general — aberrant conduction is most likely to resemble some form of conduction defect (of either bundle branch block and/or a hemiblock pattern). In contrast — VT is more likely to manifest a less well defined QRS morphology that looks different from known forms of conduction block (this concept discussed in more detail in ECG Blog #211). Exceptions exist (!) — but appreciation of this general concept goes a long way toward understanding what to look for when assessing a 12-lead tracing obtained during a regular WCT rhythm.
  • PEARL #4: Finding a prior 12-lead ECG on the patient, at a time when they were in sinus rhythm — may prove invaluable. Especially in older patients with significant underlying heart disease — "baseline" QRS morphology may look very abnormal. But IF QRS morphology in all leads during the WCT rhythm looks identical to QRS morphology on a baseline tracing when the patient was in sinus rhythm — you have proven a supraventricular etiology!
  • PEARL #5: A notable exception in which RBBB-type morphology may be seen with VT, is when there is a Fascicular VT. In such cases of this form of idiopathic VT — the impulse arises from a site in the ventricles in close proximity to either the left anterior or posterior hemifascicles. The result is a regular WCT rhythm that resembles RBBB with either LAHB or LPHB (ie, it may be difficult to distinguish between fascicular VT vs SVT with aberrant conduction from a single 12-lead tracing). The QRS complex is usually not greatly prolonged with fascicular VT (most often between 0.11-to-0.14 second). Awareness of this entity is important because despite its ventricular origin — the drug of choice for initial treatment is IV Verapamil (For more on Fascicular VT — See ECG Blog #197).




QUESTION:

  • Do you think that the 12-lead ECG shown in Figure-3 makes it more or less likely that this regular WCT rhythm is VT?

 

 

My THOUGHTS on the 12-Lead shown in Figure-3:

What follows includes basic and more advanced thoughts on the 12-lead ECG obtained during the regular WCT rhythm:

  • Although assessment of all 12 leads in Figure-3 confirms QRS widening — the QRS does not appear to be markedly widened.
  • There is no sign of atrial activity in any of the leads.
  • Although the frontal plane axis in Figure-3 is markedly leftward — the fact that the QRS complex in the inferior leads is not entirely negative reduces the diagnostic value of this ECG finding for suggesting VT (ie, there is a tiny-but-present initial r wave in each of the inferior leads) — See Simple Rule #1 in Figure-6 of the Addendum below.
  • The QRS complex in lead V6 of Figure-3 is predominantly (but not entirely) negative. As per Simple Rule #2 in Figure-6 of the Addendum below — this favors VT, but is not nearly as convincingly as it would be IF the QRS in lead V6 was entirely negative.
  • Overall QRS morphology in Figure-3 resembles RBBB (Right Bundle Branch Block) conduction — in that there is an rsr' complex in lead V1, with wide terminal S waves in lateral leads I and V6. That said — there are atypical features for RBBB conduction, including: i) The QRS complex in lead V1 is tiny, and lacks a tall, terminal R' wave (See Figure-7 of the Addendum below)andii) The r wave in lead V6 is tiny, with R wave amplitude decreasing (instead of increasing) as one moves laterally from lead V4 to lead V6.
  • The markedly leftward frontal plane axis in Figure-3 resembles LAHB (Left Anterior HemiBlock) morphology— but the r wave in the inferior leads is atypical for LAHB in being smaller in all 3 inferior leads than is usually seen with supraventricular conduction.


Putting It All Together: Assessment of the 12-lead ECG in Figure-3 during the tachycardia reveals a regular WCT rhythm at ~190/minute, without clear sign of atrial activity.

  • Statistically — We started with a ≥80% likelihood that the rhythm was VT. As per PEARL #2 — Remember that we need to prove that the rhythm is not VT, rather than the other way around.
  • Assessment of QRS morphology in Figure-3 superficially suggests bifascicular block (RBBB/LAHB). That said — the atypical features described above and lack of more marked QRS widening if anything, are in favor of a diagnosis of Fascicular VT. While impossible to rule out an SVT with either preexisting RBBB/LAHB or aberrant conduction — I'd estimate the likelihood that this rhythm is fascicular VT as approaching 90%.
  • Finding a prior ECG on this patient could be diagnostic of SVT with a preexisting conduction defect — IF QRS morphology on a prior tracing during sinus rhythm showed identical QRS morphology as was seen during the WCT rhythm in Figure-3. In the absence of a prior ECG — VT should be assumed, and the patient treated accordingly.
  • As discussed in ECG Blog #197 — therapeutic options for this patient might include IV Adenosine — IV Verapamiland/or Synchronized Cardioversion. It turns out that Adenosine was tried, but was unsuccessful. Synchronized cardioversion with 100 joules resulted in the 2 rhythms shown in Figure-4.

 

 

Figure-4: Lead II rhythm strips obtained during the WCT rhythm (Panel A) — and immediately after synchronized cardioversion with 100 joules (the RED arrow shows the point where cardioversion was applied). Panel B — was obtained moments after cardioversion.


 

 

MY THOUGHTS on the Rhythm Strips in Figure-4:

Synchronized cardioversion was successful in producing a supraventricular rhythm.

  • In Panel A — within less than 3 seconds synchronized cardioversion, we see conversion to a supraventricular rhythm with 3 narrow QRS complexes (albeit the first 2 of these 3 narrow beats are followed by PVCs).
  • A little while later in Panel B — we see 5 supraventricular beats, albeit with marked bradycardia and an irregular rhythm. It is difficult to tell whether or not a low amplitude sinus P wave might be present before the first 3 narrow QRS beats. But the KEY finding in the Panel B rhythm — is the 2nd beat, which is almost certain to be a PVC, since it is wide, very different in morphology from the narrow, supraventricular beats, and not preceded by any P wave. 
  • Isn't QRS morphology of this PVC ( = the 2nd beat in Panel B of Figure-4) very similar to QRS morphology in Panel A during the run of VT before cardioversion? 
  • PEARL #6: The finding of a PVC after cardioversion with very similar QRS morphology as was seen during the WCT further supports our assumption that the wide tachycardia was indeed VT.

 


FOLLOW-UP:

The marked bradycardia in Panel B was treated with Atropine. The result is shown in Figure-5.

  • Sinus rhythm at a regular and normal rate of 60-65/minute has returned in Figure-5 (albeit upright sinus P waves in lead II are extremely small in amplitude).
  • Fairly large Q waves are seen in each of the inferior leads. This suggests prior inferior infarction.
  • There is voltage for LVH (S in V2 + R in V5 ≥35 mm; R in V6 ≥18 mm).
  • Nonspecific ST-T wave changes are seen — although these do not appear to be acute.
  • Impression: This follow-up 12-lead ECG in Figure-5, obtained shortly after synchronized cardioversion suggests that this patient probably has underlying heart disease (ie, a prior inferior MI; LVH) — and that his coronary disease may have served as the substrate for the episode of VT. That said — at least there are no acute changes on this post-cardioversion ECG.

 

Figure-5: Following treatment with Atropine — the patient stabilized, and this 12-lead ECG was obtained.


 

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Related 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 #196 — Reviews another Case with a Regular WCT Rhythm. 
  • ECG Blog #197 — Reviews the concept of Idiopathic VT, of which Fascicular VT is one of the 2 most common types. 
  • 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 ECG Media Pearl #21 in this blog post.
  • ECG Blog #211 — WHY does Aberrant Conduction occur?


NOTE: To download my Power Point Show on this case that I presented at Jennifer Carlquist’s 5-Day EKG Challenge on May 4, 2021 — CLICK HERE

 

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ADDENDUM (5/1/2021):

I've reproduced below from ECG Blog #196 — 2 helpful figures for assessment of the regular WCT rhythm: 

 


Figure-6: Use of the "3 Simple Rules" for distinction between SVT vs VT (taken from ECG Blog #196).


 

Figure-7: Use of lead V1 for assessing QRS morphology during a WCT rhythm (taken from ECG Blog #196).







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