Defining Incomplete Right Bundle Branch Block

In my last post I featured an ECG showing a normal width QRS complex with an rsR' pattern in V1 yet no other features of Right Bundle Branch Block (RBBB) ie no terminal s wave in V5, V6, I and aVL. I called this an incomplete RBBB but pondered if indeed this was correct. Since then a bit of research has occurred.

Checking quite a few texts I found that most describe IRBBB in sparse detail. Rather RBBB is described, and a definition of IRBBB is given as: “its RBBB with a QRS from greater than 100ms and less than 120ms. So then I guess true definition of RBBB is required. It seems there are four criteria to fill to truly diagnose RBBB, they are quoted in the AHA/ACCF/HRS recommendations for standardization and interpretation of the ECG part III (1) as: 
“Complete RBBB
1.   QRS duration greater than or equal to 120ms in adults, greater than 100ms in children ages 4 to 16 years, and greater than 90ms in children less than 4 years of age.


2.   rsr’, rsR’ or rSR’ in leads V1 or V2, the R’ or r’ deflection is usually wider than the initial R wave. In a minority of patients, a wide and often notched R wave pattern may be seen in V1 and or V2.


3.   S wave of greater duration than R wave or greater than 40ms in leads I and V6 in adults.


4.   Normal R peak time in leads V5 and V6 but greater than 50ms in lead V1.


Of the above criteria, the first 3 should be present to make the diagnosis. When a pure dominant R wave with or without a notch is present in V1, criterion 4 should be satisfied.”

The same AHA/ACCF/HRS recommendations describe all these features as being required for IRBBB apart from the QRS complex width, which should between 110-120ms in adults 90-100ms in children age 16-4 and 86-90ms in children less than 4.

So now that IRBBB is defined, how does this criteria fit the ECG up for review.

Looking at criteria 1. On eyeball the QRS complex appears to be 110ms but on closer inspection the QRS is only 90ms wide.

 This fails the first criteria for IRBBB and indeed this rsR’ complex in V1 would now be considered a normal variant or would it?

WHO taskforce state (2) in relation to QRS complex width: “There is no minimal QRS duration for incomplete right bundle branch block.”

Marriott  (3) defines IRBBB QRS complex width as between 90-100ms, whereas Chan et al (4) state 80 – 110ms

The second criteria is met easily with an rsR’ in V1 with R’ wider than the initial r wave. Figure

Criteria 3 is not met as there is no distinct s wave in either lead I or V6. Figure

Criteria 4 is met as the onset of the QRS to the peak of the R’ wave is about 60ms. Figure

After all this discussion, what conclusions can be made? I guess strictly speaking this ECG can’t be called an IRBBB. I make this conclusion due to the lack of an s wave in V6 and lead I. The width criteria I think is less clear-cut as many respected authors differ in their definition. From here on in my own interpretation will reflect the WHO (2) definition on IRBBB where the QRS width in less than 120ms.

Areas to  look at in future are:

What are the clinical ramifications of IRBBB and RBBB?

Does IRBBB have any prognostic value?

Analysis of bundle branch block ECGs to practice all the diagnostic criteria.

References:

1: Surawicz, B. Childers, R. Deal, B. J. Gettes, S. (2009) AHA/ACCF/HRS Recommendations for the Standardization and Interpretation of the Electrocardiogram, Part III, Intraventtricular Conduction DIsturbances. A Scientific Statement from the American Heart Association Electrocardiography and Arrhythmias, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society. Journal of the American College of Cardiology Vol. 53, No. 11.

2: Willems, J.L. et al (1985) Criteria for Intraventricular Conduction Disturbancesand Pre-excitation WHO / International Society and Federation for Cardiology Task Force. JACC, Vol. 5, No. 6.

3: Marriott, H.J.L. Practical Electrocardiography 8th ed, Williams & Wilkins, Baltimore.

4: Chan, T.C. et al (2005) ECG in Emergency Medicine in Acute Care, Elservier Mosby, Philadelphia.

5: Surawicz, B. et al (2008) Chou's Electrocardiography in Clinical Practice 6th Ed,  Saunders Elsevier, Philadelphia.

DDD pacing with psuedo fusion

ECG taken in the midst of a bradycardia alarm.

INTRODUCTION:

I was asked to review a 12 lead ECG of a patient post abdominal surgery with a Dual Chamber Permanent Pacemaker and no myocardial ischaemic symptoms.

The indication for the 12 lead was to investigate a monitor alarm for bradycardia to 40bpm, discussion around a PPM check was beginning as medical and nursing staff were concerned the PPM was dysfunctional.

This ECG was taken in the midst of one of these alarms. The patient was asymptomatic, indeed the patient was wondering what all the fuss was about.


A quick look through the patients history/documentation showed no real details of the settings of the pacemaker.

A review of the ECG shows: 

• the rhythm which I would inelegantly call sinus rhythm with premature atrial ectopics, atrial and atrio-ventricular sequential pacing (a bit of a mouth full).
• pacemaker rate 75, but overall heart rate around 80.
• Intrinsic PR is around 230ms Measured in V4 V5
• Pacemaker AV interval is meassured at 240ms
• Incomplete RBBB pattern (? something for a future post) V1, early R wave progression, normal axis, normal width QRS complexes.
• Atrial capture of pacing is seen evidenced by p wave artifact after each atrial pacing spike, implied atrial capture is seen when atrial pacing occurs and a QRS complex follows at same interval as the intrinsic PR intervalon the 9th and the 13th.
• Ventricular capture cannot be verified, as despite ventricular pacing spikes occuring they fall on intrinsically conducted QRS complexes. Despite ventricular pacing the QRS is not deformed at all. This is called psuedofusion (Normal in ventricular pacing).
• Possibly half a mm of ST elevation in aVF and lead II but wander in the baseline could easily be the cause of this.
• T waves look unremarkable.

Judging by the ECG no evidence of a bradycardia or a dysfunctional PPM was found.

DISCUSSION:

Fusion and Psuedofusion

This is a strip showing various types of ventricular activation. The first beat is the patients own intrinsic conduction. The red arrows indicate where ventricular pacing spikes occur. The second, third, forth and fifth complexes show varying degrees of fusion. Note that the second complex is minimally distorted by activation by pacing. The third, forth and fifth complexes show increasing distortion of the QRS complex, this distortion is secondary to greater amounts of activation of the ventricular tissue via the pacemaker rather than the intrinsic conduction. The final three complexes see the ventricles completely activated by the pacemaker.

Normal  conduction in the ventricles produces a narrow QRS complex, isoelectric ST segment and normal polarity T wave. 
When the ventricles are depolarised from a stimulus from a pacemaker a wide QRS complex, discordant ST segments and T waves.
Fusion beats are a common occurance in pacing, the delivery of a pacing stimulus occuring at the same time as that of intrinsic conduction has the ventricles partly depolarised by the pacing stimulus and partly by intrinsic conduction.

Some examples of psuedofusion: Intrinsic QRS complexes not distorted by pacing.  Little to no  activation of the ventricle by the pacing stimulus. Therefore psuedofusion.

Psuedofusion is seen when a pacing stimulus is sent at the same time that intrinsic conduction occurs yet no deformation of the QRS complex occurs. This implies that little to no ventricular tissue was activated by the pacing stimulus.


Monitors and Pacing:

Monitors often have difficulties picking up changes in the ECG produced by pacing. Whilst viewing the monitor during an alarm it was noted that any time a psuedofusion complex occurred the monitor failed to register a QRS complex. The image above demonstrates that three complexes in a 6 second strip that the monitor would have missed in it's rate count. 

LEARNING POINTS:

• Pacemakers evoke fear in healthcare providers and a low threashold for PPM check exists.
• Fusion beats are common in pacing and this is an example of pseudofusion.
• Monitors are prone to being confused by pacing artifact or indeed changes in QRS morphology in response to pacing.
• Atrial capture is often difficult to appreciate on ECG although this shows big p waves and capture is implied as the 9^th and the 13^th cardiac cycle has a QRS following atrial pacing.

QUESTIONS THAT REMAIN TO ANSWER:

• Is this incomplete RBBB? No S V5, V6, or I. I need to define this a little better.

Introduction

I'm Matt, I'm a critical care nurse at a large public hospital in rural Australia. Most of my clinical experience is in cardiac nursing.

I've started this blog to act as a learning tool mostly for myself. So why is this not in a notebook and instead a public forum? Well, I thought others might find it interesting, and making my learning public will help for quality assurance (in that I'm more likely to push harder for answers and many eyes might help to pick up on when I make a mistake). 

Another reason for this blog is to try to fill a void for nursing learning that extends thought and insight beyond the basics.

I derive inspiration from the site Dr Smith's ECG Blog that stinks of quality information and insight. I can dream that I might reach that level of quality.

I hope that we can learn together and look forward to feedback. The posts are likely to be spasmotic in timing as I try to fit this in around full time work.

Regards

Matt RN