Blog #198 — Can VT Be Irregular (LBBB?)

The ECG in Figure-1 was obtained in the ED from a 60-year-old man who presented with increased dyspnea. He had a history of dilated cardiomyopathy — and was known to have complete LBBB (Left Bundle Branch Block) on previous ECGs, though no copy of any prior tracings was available at the time this patient was first seen. In view of this history — How would you interpret his ECG?

• What is the rhythm? Can you rule out VT (Ventricular Tachycardia) on the basis of this ECG?
• Is the ECG in Figure-1 typical for complete LBBB?
• Is there LVH?
• Are there hyperacute T waves suggestive of acute LAD occlusion in the anterior leads?

 

Figure-1: ECG obtained on a 60-year-old man with increased dyspnea. How would you interpret his initial ECG?

 

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NOTE #1: Some readers may prefer at this point to listen to the 5-minute ECG Audio before reading My Thoughts regarding the rhythm in Figure-1. Feel free at any time to review to My Thoughts (that appear below ECG MP-15).

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Today’s ECG Media PEARL #15 (5 minutes Audio) — Is Monomorphic VT a regular rhythm? — with attention to the 2 Caveats that emhasize how: i) Fast AFib may look regular; and, ii) Monomorphic VT is not always perfectly regular.

 

 

MY Approach to Assessing the ECG in Figure-1:

The ECG in Figure-1 is a WCT (Wide-Complex Tachycardia) rhythm.

• The rhythm is rapid — at times attaining a heart rate in the range of 160-180/minute.
• Although seemingly regular in places (See leads III and aVF) — caliper measurement suggests an irregular irregularity to the overall rhythm.
• The QRS complex is very wide (up to 0.16 second in duration in a number of leads).
• No P waves are seen.

IMPRESSION of the Rhythm: The finding of an irregularly irregular rhythm without clear sign of P waves strongly suggests that the rhythm in Figure-1 is AFib (Atrial Fibrillation) with a rapid ventricular response.

• PEARL #1: QRS morphology in the chest leads is perfectly consistent with complete LBBB (ie, predominantly negative QRS in anterior leads — with a monophasic upright R wave in lead V6). That said — it is important to appreciate that QRS morphology in the limb leads is very atypical for LBBB. This is because instead of seeing a monophasic upright R wave in lateral leads I and aVL — there is almost a null vector (ie, tiny QRS with an rsr’ configuration) in lead I — and, an rSR’ complex with small amplitude R wave in lead aVL.
• It would really help to see a prior tracing from this patient! There is significant variability in the way cardiologists interpret various conduction defects — and opinions are many as to whether QRS morphology in an ECG like the one in Figure-1 should be interpreted as “LBBB” — or — as some type of IVCD (IntraVentricular Conduction Defect). This is relevant to today’s case — because the question arises as to whether this WCT rhythm with an exceedingly wide QRS (ie, ~0.16 second) and QRS morphology atypical for LBBB might possibly be Ventricular Tachycardia?
• PEARL #2: It is important to appreciate that VT is not always a regular rhythm (this point discussed in more detail in the above ECG Media Pearl #15). That said — it would be rare for a WCT as fast, and as irregularly irregular as the rhythm in Figure-1 to be VT — so despite the atypical QRS morphology, the most likely rhythm diagnosis remains AFib with a rapid ventricular response.
• PEARL #3: Some patients with LBBB may manifest atypical QRS morphology for this conduction defect. This can be the result of: i) A relative imbalance within the left bundle branch conduction system, in which severely diseased but not completely nonfunctional hemifascicles may sometimes manifest a rightward frontal plane axis despite LBBB; and/or, ii) Scar from severe cardiomyopathy and/or prior infarction that alters the patient’s baseline ECG appearance.
• PEARL #4: Additional support that the rhythm in Figure-1 is supraventricular — is the very steep descent of anterior S waves in leads V2, V3 and V4 (albeit a bit less so in lead V1). While not definitive — the nearly straight-line descent of these anterior S waves is a common feature of LBBB conduction. In contrast — ventricular rhythms typically manifest more delay (and a significantly less steep initial descent) in anterior S waves.
• BOTTOM Line Regarding the Rhythm: I would estimate my comfort level at ~95% that the rhythm in Figure-1 is rapid AFib. I’d initiate treatment accordingly. Finding a prior tracing on this patient with identical QRS morphology could increase my confidence level to 100% that the rhythm was AFib.

 

Additional ECG Findings of Note in Figure-1:

• The usual ECG criteria for diagnosis of LVH (Left Ventricular Hypertrophy) do not hold true when there is LBBB. This is because the sequence of ventricular depolarization and repolarization is completely altered by this conduction defect. That said — virtually all patients with complete LBBB have at least some form of underlying structural heart disease. Statistically — the great majority of these patients have LVH. In the setting of LBBB — the finding of one or more very deep anterior S waves of ≥25-30 mm (in lead V1, V2 and/or V3) is strongly suggestive of LVH. In today's case — the S wave in lead V2 is >45 mm, and far exceeds this value. The S wave in lead V3 goes off the paper after 20 mm (and would doubtlessly also exceed 30 mm if the S wave was not cut off). 
• PEARL #5: Even without being told — the combination of LBBB + marked QRS widening (0.16 second) + huge anterior S wave amplitude — strongly suggests an underlying cardiomyopathy. With this in mind — the unusual QRS morphology that we see in leads I and aVL is not so unexpected.
• NOTE: The anterior T waves are huge! — attaining an amplitude of nearly 20 mm in lead V2. That said — considering how huge S waves are in these respective leads — I did not get a sense that anterior T waves were disproportionately tall. This is a judgment call. Objective assessment tools (such as modified Smith-Sgarbossa criteria) — are difficult to apply to the ECG in Figure-1, because the overly steep T wave ascent provides no hint of how much actual J-point ST elevation there might be. Finally — ST-T wave amplitude is further accentuated by the tachycardia. 

BOTTOM LINE: I suspected that the ST-T wave changes we see in the anterior leads of Figure-1 were not disproportionately increased given the huge S waves in these leads — and, I suspected these changes were unlikely to indicate an acute event (especially with no mention of chest pain). That said — I would not be ready to completely rule out an acute event on the basis of this ECG alone.

• KEY Principle: “Treat the Primary”. Regardless of whether the patient in today’s case was having an acute MI — the primary problem appears to be the rapid AFib. This should be treated first — with treatment addressing the cause of this patient’s increased dyspnea. The ECG can then be repeated — and a reassessment made.

 

Case Follow-Up: The patient’s prior ECG was found — and the conduction defect with the QRS morphology seen in Figure-1 was similar to the prior tracing. This confirmed AFib as the rhythm diagnosis. There was no acute MI.

 

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Additional Relevant ECG Blog Posts to Today’s Case: 

• ECG Blog #146 — for an example of LBBB with changes of acute STEMI.

I link to 3 additional illustrative Cases taken from Dr. Smith’s ECG Blog. For each of these posts — Please scroll down to the bottom of the page to see My Comment. These cases provide insight to assessment for acute OMI (Occlusion-based MI) in patients with LBBB (including reference when relevant to modified Smith-Sgarbossa Criteria):

• The December 16, 2019 post in Dr. Smith’s ECG Blog. 
• The April 7, 2019 post in Dr. Smith’s ECG Blog. 
• The May 24, 2019 post in Dr. Smith’s ECG Blog. 

ECG Blog #197 — Aberrant SVT vs Fascicular VT?

You are asked to interpret the ECG in Figure-1. Unfortunately — NO clinical information on this patient is available. That said — this ECG still makes for a superb discussion.

 

QUESTION: Realizing that there is no clinical information on this case — and that I do not know what happened in this case ... Which of the following choices provides the BEST answer regarding the rhythm shown in Figure-1?

 

Answers to Choose From:

• Choice A:  The rhythm is probably SVT (SupraVentricular Tachycardia) with either aberrant conduction or preexisting RBBB (Right Bundle Branch Block).
• Choice B: The rhythm is probably VT (Ventricular Tachycardia). Immediate synchronized cardioversion is indicated.
• Choice C:  Knowing the clinical history would be of little help for determining the etiology of this rhythm.
• Choice D:  Assuming the patient was hemodynamically stable — either IV Adenosine or IV Verapamil would be initial treatments of choice.

 

 

Figure-1: What is the rhythm? Unfortunately — NO clinical information is available (See text).

 

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NOTE #1: Some readers may prefer at this point to listen to the 8-minute ECG Audio before reading My Thoughts regarding the rhythm in Figure-1. Feel free at any time to review to My Thoughts (that appear below ECG MP-14).

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Today’s ECG Media PEARL #14 (8 minutes Audio) — What is Idiopathic VT? — WHY do we care? Special attention to the 2 most common forms = RVOT (Right Ventricular Outflow Track) VT and Fascicular VT. 

• NOTE: Review of the ECG features discussed in this Audio Pearl are summarized in the ADDENDUM below in Figure-2:

 

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MY Approach to the Rhythm in Figure-1:

By the Ps, Qs & 3R Approach (which I reviewed in ECG Blog #185) — the rhythm in Figure-1 is fast and Regular — the ventricular Rate is between 190-200/minute — the QRS complex is wide — and, normal sinus P waves appear to be absent.

• I can not rule out the possibility of atrial activity in this tracing. That said — I do not think the upright deflection in front of the QRS complex in lead II is a sinus P wave because: i) A rate of 190-200/minute would be exceedingly fast for sinus tachycardia in a non-exercising adult. (In general — sinus tachycardia at rates over 170/minute are not commonly seen in a non-exercising adult); and, ii) I do not see anything even remotely suggestive of sinus P waves in any other lead (Next to lead II — lead V1 is generally best for revealing sinus P wave activity, and there is no hint at all of sinus P waves in V1).
• I also can not rule out the possibility of 1:1 VA (ie, retrograde) conduction — as a thin and very deep negative deflection appears to distort the initial part of the ST-T wave, coming right after the QRS in each of the inferior leads. 
• PEARL #1: Even if 1:1 retrograde P wave activity was present — this finding does not distinguish between VT vs a reentry SVT, because both of these rhythms may conduct retrograde with a 1:1 VA ratio.

 

IMPRESSION of the Rhythm in Figure-1:

By the Ps, Qs, 3R Approach — We have described a regular WCT ( = Wide-Complex Tachycardia) Rhythm at 190-200/minute, without sign of atrial activity (at least, without any help in our differential diagnosis from the possibility of 1:1 retrograde VA activity).

• As emphasized in ECG Blog #196 — the differential diagnosis for a regular WCT rhythm without help from atrial activity includes: i) VT (Ventricular Tachycardia); ii) SVT (SupraVentricular Tachycardia) with preexisting BBB (Bundle Branch Block); iii) SVT with aberrant conduction; or — iv) Something Else! (ie, WPW). 

 

LOOKING Further — Clinical NOTES:

Unfortunately — we do not have any clinical information on this case (ie, not even the age of the patient). It’s important to emphasize that IF this patient was hemodynamically unstable in association with the rhythm in Figure-1 — then immediate cardioversion would be indicated regardless of which of the 4 diagnostic entities listed above turned out to be the etiology. For the purpose of discussion — Let’s assume the patient is and remains hemodynamically stable with the rhythm shown in Figure-1:

• QRS morphology in Figure-1 is potentially consistent with RBBB conduction because there is an rR’ (all upright) complex in right-sided lead V1 — in association with wide terminal S waves in lateral leads I and V6. Therefore — the reason for QRS widening in Figure-1 could be either preexisting RBBB — or RBBB aberration because of the rapid rate.
• PEARL #2: Although QRS morphology in Figure-1 could be consistent with RBBB conduction — there are some atypical features. These include: i) The fact that the rR’ complex in lead V1 lacks an S wave (ie, pure RBBB conduction ideally shows a triphasic = rsR’ complex in lead V1 — in which the S wave descends below the baseline); and, ii) Although the predominant negativity with very steep descent of the S wave in lead I is consistent with LPHB (Left Posterior HemiBlock) conduction — the qR pattern (ie, small-q, tall-R) expected with LPHB is absent; iii) QRS morphology in lead III is bizarre; and, iv) QRS morphology in leads V2-thru-V6 looks strangely similar (this usually doesn’t happen with RBBB conduction). BOTTOM Line: While QRS morphology in Figure-1 clearly could still represent RBBB conduction (from either preexisting RBBB or aberrant conduction) — the fact that QRS morphology manifests several atypical features negates any positive diagnostic value that might favor a supraventricular etiology. If anything — QRS morphology would seem more suggestive of a ventricular etiology.
• PEARL #3: Finding a prior tracing on this patient could be invaluable. A history of “scar” (ie, from prior infarction or cardiomyopathy) could account for RBBB conduction with atypical features. That said, in the absence of a prior tracing for comparison — Assume VT until proven otherwise!
• PEARL #4: The patient could have Fascicular VT — and THAT could account for the RBBB-like QRS appearance with the all-upright rR’ complex in lead V1 with wide terminal S waves in lateral leads. Although the most common form of Fascicular VT manifests an RBBB-like QRS appearance plus left axis deviation (which is not present in Figure-1) — variations on this “theme” exist. Therefore — it was the fact that the ECG in Figure-1 resembles RBBB but has several atypical features — that led me to suspect Fascicular VT as the diagnosis.
• PEARL #5: As per the “theme” of today’s Blog post — Fascicular VT is one of the 2 most common forms of Idiopathic VT, which is the term used to describe the approximately 10% of all VT rhythms in which the patient has VT in the absence of underlying structural heart disease. As a result — learning the age of this patient and the clinical History would be of invaluable assistance for assessing the likelihood of your rhythm diagnosis. For example — IF the patient in today’s case was a previously healthy young adult who suddenly developed this arrhythmia during strenuous exercise — the likelihood of Fascicular VT would significantly increase (For more on Idiopathic VT — See our ECG Media Pearl #14 [above] and our Summary on this topic [below] in Figure-2).

Final PEARL: Assuming the patient is hemodynamically stable — knowing the most likely diagnosis for the rhythm in Figure-1 is essential for selecting optimal initial treatment. On the basis of the above discussion — I favor Choice D as the “best” answer regarding this rhythm ( = Either IV Adenosine or IV Verapamil would be initial treatments of choice).

• The first 3 choices (A, B & C) are all suboptimal because — the atypical features for RBBB (from Pearl #2) significantly reduce the likelihood that the rhythm is an SVT — immediate cardioversion is not necessarily needed for VT if the patient is stable — and, Pearl #5 illustrates how knowing some clinical history in this patient could be of invaluable assistance for determining the likely rhythm diagnosis.
• BOTTOM Line: QRS morphology in leads I, V1 and V6 looks like a Fascicular VT (albeit without the left axis deviation that is usually seen with this rhythm). IF the clinical history was similar to that proposed in Pearl #5 (ie, a previously healthy young adult who suddenly developed this arrhythmia during strenuous exercise) — I’d probably initiate treatment with IV Verapamil, with the thought that this medication has the highest chance for success when the rhythm is Fascicular VT (plus the fact that Verapamil is also usually effective for reentry SVTs). But without this type of clinical history, and without any known history for coronary disease — I’d probably initiate treatment with IV Adenosine, with the thought that this drug is usually safe (because of its ultra-short IV half-life) — and because Adenosine will regularly convert reentry SVTs (plus it might also work if the RBBB-like pattern seen Figure-1 represented a form of idiopathic VT). 
• CAUTION — Prudence dictates remaining at the bedside during treatment, ready to cardiovert at any moment if the patient's condition deteriorates.
• 
  
• P.S. — I don’t have follow-up, and I fully acknowledge other answers are possible. YOUR comments are welcome!

 

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Acknowledgment: My appreciation to Nurul Syafika Syazwani (from Temerloh, Malaysia) for the case and this tracing.

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ADDENDUM (2/22/2021):

I summarize KEY features regarding Idiopathic VT in Figure-2.

Figure-2: Review of KEY features regarding Idiopathic VT (See text).

 

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Additional Relevant ECG Blog Posts to Today’s Case:

• ECG Blog #38 and Blog #85 — Review of Fascicular VT.
• ECG Blog #278 — Another case of a regular WCT rhythm in a younger adult.
• ECG Blog #35 — Review of RVOT VT.
• ECG Blog #42 — Comprehensive review of criteria for distinguishing VT vs Aberration.

ECG Blog #196: VT vs Aberrant? Adenosine?

The ECG in Figure-1 was obtained from a 55-year old man with a known history of coronary disease. He was hemodynamically stable at the time this tracing was recorded.

 

QUESTION: Which of the following choices provides the BEST answer regarding the rhythm shown in Figure-1?

 

Answers to Choose From:

• Choice A: The likelihood that the rhythm is VT (Ventricular Tachycardia) is approximately 50%.
• Choice B:  The likelihood that the rhythm is VT is approximately 70-80%.
• Choice C:  The likelihood that the rhythm is VT is over 95%.
• Choice D: The rhythm is more likely to be an SVT (SupraVentricular Tachycardia) with aberrant conduction.
• Choice E:  It is equally likely that the rhythm is any one of these 3 possibilities: i) an SVT with aberrant conduction; ii) AVRT (AtrioVentricular Reciprocating Tachycardia) in a patient with WPW; or iii) VT.

 

EXTRA Credit:

• Should you use Adenosine to treat the patient with this arrhythmia?

Figure-1: ECG obtained from a middle-aged man with coronary disease. What is the rhythm? (See text).

 

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NOTE #1: Some readers may prefer at this point to listen to the 13-minute ECG Audio before reading My Thoughts regarding the rhythm in Figure-1. Feel free at any time to review to My Thoughts (that appear below ECG MP-13).

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Today’s 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.

NOTE: I did not talk about Fascicular VT in today's Audio Pearl (MP-13). This is an important exception to the appearance of VT, in which QRS morphology may resemble either RBBB/LAHB or RBBB/LPHB.

• I discuss Fascicular VT (and other Idiopathic VTs) in detail in ECG Blog #197.

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MY Approach to the Rhythm in Figure-1:

The “good news” about this case — is that the patient was hemodynamically stable at the time the rhythm was recorded. This means that synchronized cardioversion is not immediately needed — which provides a moment of time to better assess the rhythm.

 

As always — I find the most accurate and time-efficient process for arrhythmia interpretation is to use the Ps, Qs & 3R Approach. As I emphasized in ECG Blog #185 (and as I repeat in Figure-4 shown in the Addendum below) — it does not matter in what sequence the Ps, Qs and 3Rs are assessed — and, I altered the sequence below for today’s tracing, based on the easiest parameters to assess for the rhythm in Figure-1. So, — I noted the following:

• The rhythm in Figure-1 is fast and Regular. The ventricular Rate is ~170/minute.
• The QRS complex is wide.
• P waves are absent.
• The 5th parameter is the 3rd R, which stands for “Related”. But since no P waves are identified in Figure-1 — there is nothing to comment on regarding this 3rd R.

 

IMPRESSION of the Rhythm in Figure-1:

By the Ps, Qs, 3R Approach — We have described a regular WCT ( = Wide-Complex Tachycardia) Rhythm at ~170/minute, without clear sign of atrial activity.

• Unfortunately — there is no simultaneously-recorded long lead rhythm strip in Figure-1. That said — a long lead rhythm strip is really not needed for the diagnosis in today’s case.
• As emphasized in today's ECG Media PEARL #13 (above) — the differential diagnosis for a regular WCT rhythm without atrial activity includes: i) VT (Ventricular Tachycardia); ii) SVT (SupraVentricular Tachycardia) with preexisting BBB (Bundle Branch Block); iii) SVT with aberrant conduction; or, iv) Something Else? (ie, WPW).
• According to the literature — statistical odds that a regular WCT without evidence of atrial activity will turn out to be VT begin at ~80% — and, increase to ≥90% if the patient is of a “certain age” (ie, middle-aged and beyond) and has underlying heart disease. Therefore, even before looking at specific ECG findings in Figure-1, such as frontal plane axis and QRS morphology — the likelihood that this regular WCT will turn out to be VT in this 55-year-old man with coronary disease is at least 90%.

 

LOOKING Further — Clinical NOTES:

The clinical reality — is that emergency providers often have to begin treatment of tachyarrhythmias before being 100% certain of the specific rhythm diagnosis. In today’s case — it would be perfectly reasonable to accept the ≥90% likelihood of VT at this point in the case — and to treat the patient accordingly.

• As already noted — the fact that the patient in today’s case was hemodynamically stable with the rhythm in Figure-1 means that electrical cardioversion was not immediately needed, and that a trial of antiarrhythmic therapy would be reasonable. IF the patient were to deteriorate at any time during assessment and treatment — THEN cardioversion becomes immediately indicated.
• A number of antiarrhythmic treatment options could be tried, the most common of which include IV Amiodarone or Procainamide. Depending on provider preference, availability, and customs/protocol at one’s institution — either of these options could be selected.
• Although Adenosine has been recommended for empiric use as treatment of a regular WCT rhythm of uncertain etiology — this drug is unlikely to be effective if the rhythm is polymorphic VT or ischemic VT. So, while it would not necessarily be “wrong” to give Adenosine to the patient in today’s case — given the known history of coronary disease in this patient, and the overly wide and amorphous morphology (not resembling any known form of conduction defect) — an ischemic etiology for this patient’s VT is extremely likely. As a result — it might best not to try Adenosine in this patient (Summary of the pros and cons of using Adenosine appears below in Figure-5 and Figure-6 in the Addendum below).

 

Can We Increase Our Certainty that the Rhythm is VT?

While initiation of antiarrhythmic treatment for presumed, hemodynamically-stable VT would be reasonable at this point (given the ~90% likelihood that the WCT rhythm in Figure-1 is indeed VT) — Wouldn’t it be better to attain an even greater degree of certainty for the rhythm diagnosis? Realizing that there are numerous criteria in the literature for distinguishing between VT vs SVT rhythms — I wanted to present my approach that has served me well over the years in terms of time efficiency and accuracy.

• I begin with attention to the “3 Simple Rules” presented in Figure-2. Applying these rules to the regular WCT Rhythm in today’s case (that we saw in Figure-1) — there is extreme axis deviation (as determined by the all negative QRS in lead aVF) — the QRS in lead V6 is almost all negative (with no more than the tiniest r wave in this lead) — and, the QRS complex is both exceedingly wide and "ugly" in a number of leads (not resembling any known form of conduction defect — with a virtually amorphous QRS in lead V1).
• Conclusion: A positive response to any one of the 3 Simple Rules would have significantly increased the likelihood of VT from our starting estimation of ~90%. The fact that each of these 3 Rules are positive should place the likelihood of VT at well over 95%. 
• KEY Point: Once familiar with the rules — it should take no more than seconds for your “educated eye” to identify that the regular, fast WCT rhythm without P waves in Figure-1 has an extreme frontal plane axis — an almost totally negative QRS in lead V6 — and, an “ugly” QRS morphology in multiple leads.

 

Figure-2: Use of the “3 Simple Rules” for distinction between SVT vs VT (excerpted from my ACLS-2013-ePub).

Beyond the Core:

The “beauty” of the 3 Rules that I illustrate in Figure-2 (and in today’s ECG Media PEARL #13) — is their simplicity and the speed with which these rules can be applied at the bedside. As a more advanced concept — I’ll add 2 additional ECG features to consider that are relevant to today’s case.

• The finding of an all-positive monophasic R wave in lead aVR during a regular WCT rhythm is virtually 100% specific for the diagnosis of VT. The reason for this — is that a monophasic R wave in lead aVR during a WCT rhythm indicates that the electrical impulse must be originating from a site in the ventricular apex, and traveling upward toward the base (ie, in the direction of lead aVR). SVT rhythms do not originate from the apex. Unfortunately — sensitivity of this finding is not high (ie, it won’t be often that you see a monophasic R wave in lead aVR during a WCT rhythm). That said — when found (as seen by the all-upright QRS in lead aVR of Figure-1) — the diagnosis of VT is confirmed!
• Assessment of QRS morphology may help! As I noted in Figure-2 — aberrant conduction almost always manifests some form of conduction defect (ie, RBBB, LBBB, LAHB, LPHB — or some combination thereof). IF a typical RBBB morphology for the QRS complex in lead V1 during a WCT rhythm can be demonstrated — then a supraventricular etiology becomes much more likely (Figure-3). In today’s case — the opposite was found regarding QRS morphology in lead V1. Thus, the nearly amorphous QRS morphology in lead V1 of Figure-1 provides further support that the rhythm here is VT.

Figure-3: Use of lead V1 for assessing QRS morphology during a WCT rhythm (excerpted from my ACLS-2013-ePub).

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Relevant ECG Blog Posts to Today’s Case:

• ECG Blog #220 — Walking Step-by-Step through a detailed Case Study of a regular WCT rhythm (Audio Pearl on what is Hemodynamic Stability?).
• ECG Blog #42 — Comprehensive review of criteria for distinguishing 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. 
• ECG Blog #38 and Blog #85 — Review of Fascicular VT.
• ECG Blog #35 — Review of RVOT VT
• 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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ADDENDUM (2/20/2021):

• I like to frequently emphasize my systematic approach to rhythm interpretation. Relevant links to audio — video — and pdf review of this topic are found on my ECG Blog #185. I reproduce the 5 KEY elements to my approach below in Figure-4.
• Adenosine is a wonderful drug for emergency treatment of reentry SVTs. It is also effective for a selected number of adenosine-responsive VT rhythms (primarily in younger adults who do not have underlying heart disease). Because of its ultra-short half-life following IV administration — it is usually safe when given empirically to patients in whom the etiology of a WCT rhythm is unknown. That said — side effects can occur, and these are not uniformly short-lived. Therefore — the drug is probably best avoided for WCT rhythms for which it has little to no chance of being effective (ie, polymorphic VT; ischemic-etiology VTs). In Figure-5 and Figure-6 — I reproduce the section on these pros and cons for use of Adenosine (excerpted from my ACLS-2013-ePub).

Figure-4: Review of the 5 KEY elements in the Ps, Qs & 3R Approach to systematic rhythm interpretation (See text).

Figure-5: Pages 1 and 2 on use of Adenosine (excerpted from my ACLS-2013-ePub).

 

Figure-6: Pages 3 and 4 on use of Adenosine (excerpted from my ACLS-2013-ePub).

 

Blog #195 — Are P Waves Related to the QRS?

The long lead II rhythm strip shown in Figure-1 was obtained from a previously healthy 27-year-old man who presented with dyspnea.

 

QUESTIONS:

• What is going on with the rhythm in Figure-1?
• Will this patient need a pacemaker?
• Extra CREDIT: There is a special name for the phenomenon that we see in this rhythm. Do you know what it is?

 

Figure-1: Lead II rhythm strip, obtained from a 27-year-old man with dyspnea (See text).

MY Approach to the Rhythm in Figure-1:

I find 2 simple steps tremendously facilitate both explaining as well as interpreting complex arrhythmias. These 2 simple steps are: i) Numbering the beats; and, ii) Highlighting P waves with ARROWS (Figure-2):

• Use calipers! As I continually emphasize — the EASIEST way to instantly become better (and faster) at analyzing complex arrhythmias is to use calipers. P waves are obvious in front of some but not all of the QRS complexes in Figure-2. By using calipers — I instantly remove any doubt that the tiny (partial) deflections I see deforming the onset of QRS complexes #2 and 6 are indeed P waves that are partially hidden by near-simultaneous occurrence of these beats.
• Isn't it interesting how the PR interval continuously changes from one-beat-to-the-next in Figure-2?

 

Continuing systematically to assess the rhythm in Figure-2 by the Ps, Qs & 3R Approach (See ECG Blog #185): 

• The QRS is narrow (at least in this single monitoring lead).
• The ventricular rhythm looks fairly (but perhaps not completely?) regular at a rate between ~50-55/minute. 
• And, as mentioned — the PR interval continuously changes, so there is no fixed relationship between P waves and neighboring QRS complexes.

 

Figure-2: I’ve labeled the rhythm in Figure-1 by highlighting P waves (RED arrows) and numbering the beats (See text).

 

MY Approach to this Rhythm (Continued):

I wondered WHY the PR interval was continually changing in Figure-2?

• Time to use calipers again! I wondered IF the P-P interval in this rhythm remained constant — and also IF the R-R interval remained constant?
• For clarity — I show my caliper measurements in Figure-3 for both the P-P interval (RED numbers) and the R-R interval (BLUE numbers). Note that neither the atrial nor ventricular rates remain completely constant in Figure-3. Instead, there is slight variation in both intervals that differ from each other in the way they are changing.

 

Figure-3: I’ve measured the P-P and R-R intervals in Figure-2 (See text).

Putting It All Together:

As per the Ps, Qs & 3R Approach — the rhythm in today’s case is fairly (but-not-completely) regular, within a rate range for the ventricular rhythm of between ~50-55/minute. The QRS complex is definitely narrow in this single lead II rhythm strip. P waves are present — but they are not related to neighboring QRS complexes (because the PR interval continually changes throughout the tracing).

• The fact that the PR interval in Figure-2 is constantly changing — tells us that many (if not all) of the P waves are not conducting. Clearly, the PR interval before beats #1, 2, 4; 6, 7 and 8 is too short to conduct. I thought the PR interval before beat #5 was slightly shorter than the PR interval before beat #3. Whether either of these P waves are conducting is debatable — and probably not possible to determine with certainty from this single rhythm strip. Regardless — the “Take-Home” message is that there is AV dissociation for either part or all of the rhythm shown in Figure-2.
• Because the QRS complex in Figure-2 is narrow and not the result of sinus-conducted beats (with possible exception of beats #3 and 5) — most QRS complexes in this tracing are arising from the AV node (ie, they are junctional beats).

 

NOTE: Although we have established the presence of AV dissociation for either a part (or all) of the rhythm in Figure-2 — AV Dissociation is never a “diagnosis”. Instead — it is merely a description of the fact that at least temporarily, regular P waves are not related to neighboring QRS complexes.

• As discussed in detail in ECG Blog #192 — there are 3 Causes of AV Dissociation to consider. These are: i) 2nd- or 3rd-degree AV Block (in which one or more P waves that should conduct do not conduct); ii) AV dissociation by “Usurpation” (in which an accelerated junctional rhythm takes over the pacemaking function); and/or iii) AV dissociation by “Default” (in which slowing = “default” of the SA nodal pacemaker allows a junctional escape pacemaker to emerge).
• There is no evidence of any AV block in today’s rhythm. This is because none of the P waves (RED arrows) that fail to conduct — had a chance to conduct, since the PR interval was too short. This is not to say that there might not be some degree of AV block — but only to say that the rhythm in Figure-2 is too short to answer this question (because we never see P waves occurring at points in the cardiac cycle when they should be expected to conduct, yet fail to do so).
• The cause of AV dissociation in Figure-2 is also not "usurpation". Looking at the R-R intervals that I measured (BLUE numbers in Figure-3, that range from 5.7-to-6.1 large boxes in duration) — this corresponds to a ventricular rate between ~49-to-53/minute — which falls well within the usual junctional escape rate of 40-60/minute in adults. Thus, there is no "usurpation" — because the junctional escape rhythm is deinitely not accelerated!

 

This leaves us with “default” ( = slowing of the sinus pacemaker) as the cause of the AV dissociation that we see in today’s rhythm. It is because the SA node slows — that a junctional escape rhythm is able to emerge.

• That said — there is a difference between today’s rhythm, and the much more common variation of AV dissociation by “default” that we saw in ECG Blog #192. Most of the time, escape rhythms are surprisingly regular — as was the junctional escape rhythm in Blog #192.
• Instead, in today’s case — the P-P and R-R intervals that I measured in Figure-3 (RED and BLUE numbers in this Figure) continually vary. Yet despite this — a 1-P wave to 1-QRS complex ratio persists, albeit with P waves moving in-and-out of the QRS.

 

This phenomenon of nearly equal sinus and junctional escape rates that continue to vary slightly, yet somehow maintain a close (yet slightly variable) proximity of P wave to QRS over time is known as isorhythmic AV dissociation. 

• As I discuss in today’s ECG Media PEARL #12 (6:40 minutes Audio) — this unusual form of AV dissociation is defined by its name. Both pacemakers are “isorhythmic” (ie, nearly equal rates for sinus P waves and the junctional rhythm) — and — there is AV “dissociation” (ie, the atria and AV node beat independently from each other — and there is no conduction of sinus impulses as long as the rhythm lasts).
• NOTE: The colorful term, “accrochage” (from the French word for “hanging on” or “hooking” onto something) — has often been used to refer to the uncanny pursuit of P waves to neighboring QRS complexes, despite slight variation in the rates of these P wave and QRS rhythms. The less colorful term, "synchronization" is then preferred when the phenomenon of isorhythmic AV dissociation is longer lasting.

CLINICALLY — The significance of AV dissociation (be it isorhythmic or otherwise) depends on the clinical setting in which it occurs. 

• As emphasized earlier — there is no evidence of any AV block in today’s tracing. Assuming this lack of evidence for AV block continued with additional monitoring — the clinical course of this 27-year old man’s isorhythmic AV dissociation is most likely to be benign.
• NOTE: AV dissociation by “default” is not uncommon among otherwise healthy, athletic individuals — because predisposing sinus bradycardia is common with increased resting vagal tone. Having such individuals exercise briefly is usually enough to sufficiently increase the sinus rate — which when the rhythm is benign, will result in sinus P waves regaining control of the rhythm (and overriding the resting junctional escape rate).
• I suspect that the patient’s dyspnea in today’s case is not related to his cardiac rhythm. There is no evidence to suggest that a pacemaker will be needed for this patient.

—  —

Today’s ECG Media PEARL #12 (6:40 minutes Audio) — reviews the entity known as isorhythmic AV Dissociation.

 

 

Proposed Laddergrams for Today’s Case:

I conclude this case by proposing 2 potential laddergrams for today’s rhythm.

• I suspect the laddergram I’ve drawn in Figure-4 is more likely — because most of the time with true isorhythmic AV dissociation, for as long as this phenomenon lasts — sinus and junctional pacemakers continue to discharge within the Absolute Refractory Period of the other, resulting in non-conduction of all sinus P waves.
• That said, because we have not seen a prior tracing from this patient in which he was normal sinus rhythm — we have no idea of what his “normal PR interval” is when sinus beats are conducted. It is therefore impossible to know if the PR interval of 0.14 second that is seen before beat #3 is (or is not) sinus-conducted (Figure-5).
• In Theory — true isorhythmic AV dissociation in which there is no conduction of any sinus impulses, will continue until a significant change in either the sinus or junctional rate occurs.
• Practically Speaking — it does not matter if beat #3 is or is not a sinus-conducted beat. Regardless — the underlying mechanism of today’s rhythm is sinus bradycardia that results in a period of isorhythmic AV dissociation with a junctional escape rhythm — and which in an otherwise healthy young adult, is almost certain to be benign.

 

Figure-4: Proposed Laddergram #1 — which I think is the more likely mechanism, since “capture” beats are generally not seen with true isorhythmic AV dissociation until a significant change in rate of either the atrial or ventricular rhythm occurs (See text).

 

Figure-5: Proposed Laddergram #2 — in which the QRS complex preceded by the longest PR interval (ie, beat #3) might be a sinus-conducted beat. It’s impossible to rule this in or out, however — without knowing what this patient’s “normal PR interval” is during a normal sinus rhythm (See text).

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Acknowledgment: My appreciation to Feroz Haroon (from Srinagar, Kashmir, India) for the case and this tracing.

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