A Closer Look at Right Bundle Branch Block (RBBB)

Jerry W. Jones, MD FACEP FAAEM


I once wrote an article about “rabbit ears” and RBBB and posted it on my blog (https://medicusofhouston.com/dr-joness-ecg-blog/). To this date it has been the most read article I have produced. So, let’s take a closer look at RBBB. 

The right bundle branch courses down the wall of the interventricular septum on the right ventricular side. Its course is superficial at some points, so it is very susceptible to injury by central venous lines or stretching (dilatation) of the right ventricle.

The diagram on the left shows both bundle branches (right – yellow, left – red). With the right bundle branch blocked up high (dotted line), the atrial impulse travels down the left bundle branch into the anterior and posterior fascicles. The left ventricle is depolarized normally and at its usual speed.

The first portion of the left ventricle to be depolarized is the mid-septum on the left side. This is normal. The depolarization of the interventricular septum is initiated by either the posterior fascicle or a septal fascicle. Let’s not concern ourselves with the septal fascicle.

Here is where the difference from a normal beat begins. The depolarization of the interventricular septum from left-to-right is normally met by depolarization from the right ventricle from right-to-left. When that happens, it only takes about 32 msec to depolarize the entire width of the septum at the level of the mid-septum. Without the depolarization coming from the right side, it will take about 60 msec for one-way, full-thickness depolarization of the septum at the mid-septal level. That’s if the myocardium is very healthy! Otherwise, it can take up to 110 msec if the myocardium is not so healthy (ischemic, fibrous deposits).

Let’s look at Lead V1. The first part of the QRS is exactly what we would expect of a normal V1 – a small r wave followed by a deep S wave. Now let’s take an even closer look at Lead V1…

I chose this particular QRS because it begins on a grid line. When we look at the first two deflections of this complex (small r and deep S), we see that the r begins directly on a grid line and then the S wave returns to the baseline exactly 60 msec later (1.5 small squares). Anything sound familiar?

Now we have a large R′. It appears to be just under 60 msec. The R′ is the depolarization of the right ventricle occurring after depolarization of the left ventricle – instead of simultaneously with it.

We know that the depolarization of the right ventricle cannot begin until the septum has been completely depolarized in the mid-septal area from left-to-right. Now, how is the right ventricle depolarized? Is it via that portion of the right bundle branch and His-Purkinje system located distal to the block or is it by cell-to-cell conduction? Or is it a combination of both? The answer is… YES! All three scenarios are possible.

If the impulse coming from the left ventricle enters the right bundle branch immediately, the QRS duration will be at or just slightly longer than 0.12 seconds. Bear in mind, this has no effect on the first portion of the QRS representing left ventricular depolarization. It will remain normal-appearing no matter which route the depolarization of the right ventricle takes. If the impulse does not enter the right bundle branch, but instead travels by cell-to-cell conduction, the R′ will be much wider because depolarization of the right ventricle will take much longer. If the impulse begins depolarizing the right ventricle in a cell-to-cell manner, but then manages to enter a conducting fiber, the QRS duration will be intermediate between the other two scenarios.

We usually look at Lead V1 when we diagnose a right bundle branch block because it is the most rightward of the routine precordial leads. Also, it is the best lead for differentiating between right and left. But it is NOT the most rightward lead on the ECG! Quite the contrary! Lead aVR is by far the most rightward lead and it will always resemble Lead V1 during a right bundle branch block.

As they say on the infomercials, “But wait! There’s more!” Lead V1 and aVR are not the only right-sided leads on the standard ECG. Lead III is also a right-sided lead and will sometimes resemble Leads V1 and aVR – but not always. At least, when it does resemble V1 and aVR, you’ll know why.

The R′ in the right-sided leads is – as you surely most know by now – due to the late activation of the right ventricle. The left-side leads also reflect this, but in a different way. Whereas the right-sided leads see that terminal activation as a wave front traveling toward them, the left-side leads see the same wave front traveling away from them. Thus, the left sided leads inscribe a wide, slurred S wave. You will see this in Leads I, aVL and V6. Just having a terminal S wave is not enough – that S wave must be slurred (widened). Many experts feel that the S wave should be as wide as the R wave.

If you looked closely, you will have noticed that there appears to be a significant QT prolongation. The QTc states 484. Yet the ECG machine does not report a prolonged QT as an abnormality. Here’s the problem: prolongation of the QRS interval due to a bundle branch block confuses the calculation of the QT interval. The ECG machine read the QRS duration as 124 msec. If we were to subtract 24 msec from 484 msec, we would have 460 msec. Elevated a bit but in itself not likely to cause any problems for a male. But is it that simple? Can we do that? I don’t think anyone has proved that it is feasible. Others have developed elaborate formulae to adjust for bundle branch block, but to my knowledge none have been accepted by most experts.

















Lagniappe (if you lived or went to school in New Orleans, you’ll know what that means):

Most bundle branch blocks are not actually blocks. What occurs is that one bundle branch is very slow compared to the other. When a bundle branch can conduct rapidly enough to cross the septum before the impulse arrives in the opposite ventricle, it will then begin activation of that ventricle. Let’s say the right bundle branch is slow, and it often really is slow. The left bundle activates the left ventricle and then crosses over the septum. Once it reaches the right side, it enters the right bundle branch and conducts in BOTH DIRECTIONS. Of course, the impulse traveling retrogradely up the right bundle branch collides with the late impulse traveling down the right bundle and they extinguish themselves, leaving that area of the right bundle branch very refractory. Meanwhile, the impulse that traveled from the left ventricle and then conducted antegrade (forward) down the right bundle branch and conduction system has completed depolarization of the right ventricle. But what happens with the next beat as the impulse begins down the right bundle branch? It’s going to run into that area of refractoriness – likely absolute refractoriness – and activation of the left ventricle first and right ventricle last will be perpetuated.

Think about it.






Location: Houston, Texas

Comments

Post a Comment

Popular posts from this blog

Image
  Analyzing an Acute MI “Jones’s Rule” and Primary Repolarization Changes Jerry W. Jones, MD FACEP FAAEM Figure 1 This is another 12-lead ECG randomly selected from my collection. There is a bit of baseline wander, but that’s life! It was recorded on a 68 y/o Hispanic female in the emergency department who was complaining of chest pain. There is no other information about her. First, the absolute basics. We can see by the upright P waves in leads I and II that sinus rhythm is present. The pos/neg biphasic P wave in Lead V1 is also supportive of sinus rhythm. The P wave in Lead V2 is basically isoelectric – but that’s OK, as long as it isn’t inverted or biphasic. There is 1:1 sinoatrial conduction and the P-R intervals are normal and remain the same. The rate is quite variable and may represent a sinus arrhythmia. Also, as we will see in a moment, there is also a good reason for increased parasympathetic influence on the rate. No apparent lethal dysrhythmias and no blocks are not...
Read more
Image
  Notes on a Randomly-Selected ECG Jerry W. Jones, MD FACEP FAAEM Figure 1 What is the rhythm on this ECG? Don’t be too quick to respond because I just asked you a trick question! Which rhythm are we discussing – the atrial rhythm or the ventricular rhythm ? Although this looks like a “single” ECG, it is really two ECGs – an atrial ECG and a ventricular ECG – one superimposed upon the other. Let’s begin with the atrial rhythm. Do you see any P waves? I don’t. That – by definition – is either atrial fibrillation , sinus arrest or third degree SA block . Now let’s consider the ventricular rhythm. It appears irregular . It is always best to assume that a ventricular rhythm that is based on an ectopic junctional or ventricular escape pacemaker will be very regular – even though it may be very slow. That isn’t always the case, but it will be about 99% of the time in my experience. OK… let’s put these two observations together: if the atrial rhythm (or lack of an atrial ...
Read more
Image
  Are you treating myocardial infarctions? Why? That's DEAD tissue! You should be treating myocardial ischemia! What's the difference between ST elevation and ST depression? Does ST depression ALWAYS represent a subendocardial ischemia? Does  ST elevation ALWAYS  represent an acute transmural ischemia? Which blood test do you use to confirm an acute transmural ischemia...         ...troponins, or a CK-MB? If you base you diagnosis of an acute transmural ischemia on the presence of ST elevation according to the STEMI protocol, then you are basing your diagnosis on a CK-MB, because that's the test that was used to "prove" that the ST deviation was or was not a STEMI! The STEMI protocol was based on just ONE article that used CK-MB assays as proof of acute transmural ischemia. Is there a problem with that? Well, no... if you don't mind missing about 25% of acute transmural ischemias that should have gone directly to the cath lab but instead were...
Read more