T W memory in LBBB-aberrancy

What is your  ECG dx? 

Remastered using @PMCardio App

Image 1 - Image case

A-SR/SB, dextrocardia

B-SR/SB, anterior wall ischemia

C-SR/SB, intermittent WPW pattern

D-SR/SB, LBBB-aberrancy, TW memory, poss lead reversal

AIVR/VT or Aberrancy?

Pt admitted due to SOB due to CHF. Is this accelerated idioventricular rhythm/ventricular tachycardia (AIVR/VT) or aberrancy?

WCT - VT or Aberrancy?

Image 1-  ECG case

A 65 yo with history of HTN admitted due to aortic aneurysm.

Is this VT or aberrancy? Why?

Image 2 - ECG case marked

It is indeed difficult to tell with certaintly the difference from ventricular tachycardia (VT) and aberrant beats using rhythm strips. The famous Brugada algorithm used the 12lead ECG. It is wrong to use the ventricular rate to descriminate VT from aberrancy bec the rates overlap. 

V1 can be used on the assumption that V1 is on the right location (4th right ICS parasteral line). However, in reality most V1 are placed in the wrong spot.

Wide QRS tachycardia WCT) can be generally grouped into right bundle branch block (RBBB) or left bundle branch block (LBBB) morphology. This is based on the termial deflection of V1. A LBBB WCT is one with a terminal negative deflection in V1 and RBBB is then a positive

terminal deflection.

The presented case is a RBBB WCT. It has the "Rabbit ears" R>R' (blue arrow). This morphological criteria is part of the Wellen's criteria for RBBB VT. 

Another feature that can be seen here is a fusion beat (red arrow). This is highly diagnostic of VT. Those complexes are a blend of 2 sources.

Based on those findings (Rabbit ear RBBB and fusion beats), we can say that this WQRST is ventricular tachycardia.

#675

Fast Rhythm: VT or reentry?

VT or reentry?

Image 1 - ECG case

This is a regularly irregular rhythm at a rate of 100-180's. There are wide QRS beats RBBB and LBBB morphology.

Image 2 - Sinus P waves marked

We can still march the P waves (red). So, the rhythm is still sinus but interrupted by 2 beats of QRS with RR cycle length (CL) of about 320 ms.

Image 3 - Ladder diagram

If we go back to the previous strips, we know that there are premature or there are junctional beat that is trying to reenter (echo beats). So, we are looking at a reentry phenomenon (if there are only one or 2 complexes). If it continues then it is called reentry tachycardia (which is not the case here). Of note is that the reentry complexes are conducted with aberrancy.

This strip is from the same patient in cases:

http://goo.gl/GOUIpZ

https://goo.gl/3NUqWD

https://goo.gl/8VFozh

#502 

The "K. Wang Logic" of WCT

Here is a practical way of knowing if WCT is VT or SVT with aberrancy.

- From Atlas of Electrocardiography 2013 by Dr. K Wang

Wide QRST: VT or not?

Vignette: A 60 yo patient with history of HTN and DM admitted due to sepsis. Monitoring captured this. What is the ECG interpretation?

Image 1 - Image  case in full disclosure

Concealed Transeptal Conduction

Image 1

To the left is a left bundle branch block (LBBB) morphology at cycle length ~ 800 ms with a PRI ~ 160 ms. Same thing is to the right with normal QRS duration.

It can be said that the LBBB in this case is not a fixed phenomenon. There is normalization after a PVC (coming from the LV - RBBB morphology). 

Persistence of BBB at lower cycle length and termination by a PVC

The persistence of BBB at lower cycle length (here ~ 800 ms) can be due concealed transseptal conduction. Concealed simply means you cannot see it in surface ECG but can be recognized from its effect on the subsequent impulse. The LBB here is not fixed so something is making the LBBB. 

In this tracing we may not know the initiating event of the LBBB but it continued. Its perpetuation may be due to impulse coming from the right bundle that penetrated (transeptal-retrograde) and collided with the incoming (antegrade) impulse of the left bundle.

The abrupt recovery was due to the PVC that excited the left bundle early and allowed more time for it to recover ("peel back refractoriness"). 

Image 2

Ref: 

Fisch C., Zipes DP and McHenry PL. 1973. Rate Deependent Aberancy. Circ 48:714-724 (http://circ.ahajournals.org/content/48/4/714.ful l.pdf+html)

Fisch C and Knoebel SB. 2000. Electrocardiography of Clinical Arrhythmia. New York. Futura Publishing Co.

Neiger JS and Trohman RG. Differential Diagnosis of Tachycardia with a Typical LBBB Morphology. WJC 3(5):127-134

http://www.wjgnet.com/1949-8462/full/v3/i5/127.htm

Acceleration-dependent aberrancy

A 73 yo is admitted due to shortness of breath. Is this ventricular tachycardia (VT)?

Figure 1 - ECG case

Aberrancy

ECG case # 1

This was captured on telemetry on a patient admitted for altered mental status. Do you agree with the machine that there is a premature ventricular complex (PVC)?

Figure 1 - ECG case # 1

When you look at a "funky" arrhythmia, always remember that there must be a unifying explanation that is causing that "funkiness". In this first case, the arrhythmia can be explained on what happens to a premature atrial complex (PAC)?

The first 3 premature atrial complexes (PAC's) are easy to catch. The wide QRS complex with a right bundle branch block or  RBBB morphology (predominantly positive QRS complex in V1)  is often labeled as a premature ventricular complex (PVC) but it is not. The non-conducted PAC's on the last 3 complexes are challenging for those not working in telemetry floors.

The 3 fates of a PAC. The first 3 PAC's (red arrows) which are QRS #s 2,4 and6 are conducted with a normal QRS morphology. The 4th PAC (black arrow) which is QRS #8 is conducted with a right bundle branch block (RBBB) configuration. The last 3 PAC's (green arrows) which are after QRS #s 9,10 and 11 are not conducted. A PAC that conducts through the AV node but finds the right bundle branch refractory will conduct with a RBBB morphology (conducted with aberrancy).

 ECG case # 2 - Is this patient having frequent PVC's?

Figure 2 - ECG case # 2

The intrinsic rhythm is atrial fibrillation with frequent wide QRS complexes (RBBB morphology) after a long R to R cycle. The machine read it as PVC in trigeminy and ventricular tachycardia (VT) but this is Ashman's phenomenon and the wide QRS beats are not VT but they are aberrant beats due to the same phenomenon.

 ECG case # 3 - Do you believe the machine that the patient is having VT?

 

Figure 3 - ECG case # 3

When the heart rate goes-up, VT alarm is always triggered. There is intermittent/transient LBBB as the heart rate increases but as the rate decreases the narrow QRS would appear. This is acceleration-dependent LBBB.

ECG case # 4 - Is that ventricular escape?

 

Figure 4 - ECG case # 4

The intrinsic rhythm is atrial fibrillation. As the ventricular rate decreases, the QRS widens (left bundle branch block or LBBB morphology). This is deceleration-dependent LBBB.

 Aberrant ventricular conduction

 

A narrow QRS complex is the considered normal and it requires highly synchronous activation of the ventricles which is made possible though the rapidly conducting His-Purkinje system (HPS).

Figure 5 - His-Purkinje system

The term aberrancy (aberration or aberrant intraventricular conduction)  is used to describe transient bundle branch block (BBB) and does not include QRS abnormalities caused by preexisting BBB, preexcitation, or the effects of drugs/electrolyte. The mechanism of aberration can occur anywhere in the His-Purkinje system. The transient BBB is due to impulse transmission of a supraventricular beat during period of physiologic refractoriness and/or depressed conductivity. The supraventricular electrical impulse is conducted abnormally through the ventricular conducting system. This results in a wide QRS complex that may be confused with a ventricular ectopic beat or PVC or VT (if 3 or more).

 An aberrant beat can have RBBB or LBBB morphology. Simplistically, a  RBBB is recognized by a QRS duration ≥ 120 ms with a predominantly positive portion in V1. LBBB has a QRS duration of ≥120 ms with a predominantly negative  terminal portion in V1.

Figure 6 - V1 lead - RBBB pattern in A and LBBB pattern in B

Aberration caused by premature excitation (ECG case # 1)

 

In the normal heart, aberration following a PAC is due to excitation prior to full recovery of transmembrane action potential (TAP) during the period of voltage-dependent refractoriness. The most common morphology is RBBB because of the longer refractory period of the RBB. This is what is seen in the ECG case # 1.

Figure 7 - The RBB has a longer refractory period compared to the LBB

 Here is another example of PAC conducted with aberrancy.

 

Figure 8 - The rhythm is sinus with PAC in bigeminy conducted with narrow QRS, non-conducted and conducted with aberrancy with RBBB morphology (PAC's marked in red arrows)

 Ashman's Phenomenon (ECG case # 2)

 

Figure 9 - Ashman's phenomenon

In 1947, Gouaux and Ashman noticed that during atrial fibrillation, when a relatively long (R to R) cycle is followed by a relatively short cycle, the beat that ended the short cycle will be conducted with aberrancy. The reason for this is that the refractory period of the ventricular conduction system varies with rate and is directly proportional to the preceding cycle; a longer cycle lengthens the ensuing refractory period and if a considerably shorter cycle follows, the beat ending is likely to be caught in the lengthened refractory of one of the bundle branches.

Figure 10 - Ashman phenomenon - In A, QRS # 3 or R3  (PAC)  is conducted normally because the it is occurred outside the  refractory period of the His-Purkinje system. In B, R3 (PAC) is conducted with aberrancy or RBBB morphology because it landed while the His-Purkinje system is still refractory. The lengthening of the refractory period is due to the lengthening of the preceding RR cycle.

Rule of Bigeminy

Now that you've heard of Ashman's phenomenon and you would assume that a long-short cycle will have an aberrant beat. Let me confuse you a little bit. There is such a thing called the "rule of bigeminy" which says that a long R to R cycle tends to precipitate a ventricular extrasystole or a PVC. So, a long-short cycle sequence cannot be used to favor aberrancy or a PVC because it favors both. To differentiate aberrancy from PVC, we are to rely on the shape/morphology of the QRS.

V1 and V6 Morphology

Lead II is the popular lead used in monitoring. However, we cannot use this lead in differentiating aberrancy from a ventricular beat. The best lead/s are V1 and V6. Yes, there can be V6 in telemetry. A six-wire system will have the V6 or seen as Vb on telemetry boxes. V1/V6 are the best leads but if they are not  in the right location then they are useless. Please make it a practice to check lead placement location.

Figure 11 - V1 and V6 Morphological criteria for VT and aberrancy

ECG case #2 had an rsR' morphology favoring aberrancy.

Figure 12 - ECG case # 2 showing rsR' morphology in V1

Coupling Interval

Coupling interval refers to the interval between the wide QRS complex and the preceding QRS of the normal beat. A fixed coupling interval favors the diagnosis of PVC than aberrancy. ECG case # 2 had a variable coupling interval favoring aberrancy.

Figure 13 - ECG case # 2 showing variable coupling interval (in millisecond) as measured in V1

Aberration caused by heart rate acceleration/acceleration-dependent aberrancy(ECG case #3)

The refractory period of the HPS shortens as the heart rate increases. So, normal conduction is preserved (narrow QRS during tachycardia). On the other hand, acceleration-dependent aberration is a result of the failure of the refractory period to shorten, or in some cases to lengthen, in response to acceleration in heart rate. 

The effective refractory period (ERP) of the right bundle (RB) normally shortens at a faster rate to a greater degree than that of the left bundle (LB). This explains the more frequent RBBB aberration at longer cycle lengths (longer RR interval) and LBBB aberration at shorter cycle lengths.

Acceleration-dependent aberration differs in many respects from aberration in normal hearts and is a marker of some type of cardiac abnormality. It has the following behavior:

• ·         frequently appears at relatively slow heart rates (less than 70beats/min)

• ·         often displays left bundle branch block configuration

• ·         appears after several cycles of accelerated but regular rate / or appears with gradual rather than abrupt acceleration of the heart rate and at CL shortening by less than 5 milliseconds

Because the changes in RR interval is gradual, this is difficult to recognize in a short ECG strip. So, a review of saved telemetry data will capture the transition from a narrow QRS to wide or aberrant beats.

When the heart slows down, the aberrancy often persist. The persistence of aberrancy can be due concealed transeptal conduction. Normal conduction (normal QRS duration) is seen later as the heart rate slow down more.

Figure 14 - Concealed transeptal conduction

Aberration caused by heart rate deceleration/bradycardia-dependent aberrancy(ECG case#4)

ECG case # 4 is an example of bradycardia-dependent aberrancy. A LBBB-shaped QRS can be seen as the heart rate decreased. This is not commonly seen. The most widely accepted mechanism of deceleration-dependent aberrancy is the gradual spontaneous reduction of the phase 4 of the transmembrane action potential in an abnormal cells or group of cells. During the long pause, the His-Purkinje system begin to depolarize to reach action potential. By the time a supraventricular impulse arrives, not all His-Purkinje system is negative enough to propagate the impulse and creating an aberrant beat.

Looking at the V1 morphology of V1 the nadir of S is less than 60 ms.

 

Figure 15 - ECG case # 4 showing nadir of S less than 60 ms favoring aberrancy